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Journal articles on the topic 'Heterologous Immunity'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

CLARK, I. A. "Heterologous immunity revisited." Parasitology 122, no. 7 (May 2001): 51–59. http://dx.doi.org/10.1017/s003118200100734x.

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CLARK, I. A. "Heterologous immunity revisited." Parasitology 122, S1 (March 2001): S51—S59. http://dx.doi.org/10.1017/s0031182000017340.

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Heterologous immunity, or protection by one invading organism against another across phylogenetic divides, has been recognised for decades. It was initially thought to operate largely through enhancement of phagocytosis, but this explanation became untenable when it was realised it worked extremely well against intraerythrocytic protozoa and killed them while they were free in the circulation. Clearly a soluble mediator was called for. This review summarises the logic that arose from this observation, which led to a wider appreciation of the roles of pro-inflammatory cytokines, and then nitric oxide, in the host's response against invaders, as well as the ability of these mediators to harm the host itself if they are generated too enthusiastically. This has led to a discernable pattern across heterologous immunity as a whole, and its lessons influence a range of areas, including vaccine development.
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3

Welsh, Raymond M., Jenny W. Che, Michael A. Brehm, and Liisa K. Selin. "Heterologous immunity between viruses." Immunological Reviews 235, no. 1 (April 28, 2010): 244–66. http://dx.doi.org/10.1111/j.0105-2896.2010.00897.x.

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4

Rehermann, Barbara, and Eui-Cheol Shin. "Private aspects of heterologous immunity." Journal of Experimental Medicine 201, no. 5 (March 7, 2005): 667–70. http://dx.doi.org/10.1084/jem.20050220.

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Clinical manifestations of viral infections are highly variable, both in type and severity, among individual patients. Differences in host genetics and in dose and route of infection contribute to this variability but do not fully explain it. New studies now show that each subject's history of past infections individualizes the memory T cell pool. Private T cell receptor specificities of these preexisting memory T cell populations influence both disease severity and outcome of subsequent, unrelated virus infections.
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Welsh, Raymond M. "Private specificities of heterologous immunity." Current Opinion in Immunology 18, no. 3 (June 2006): 331–37. http://dx.doi.org/10.1016/j.coi.2006.03.002.

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6

Pusch, Emanuel, Harald Renz, and Chrysanthi Skevaki. "Respiratory virus-induced heterologous immunity." Allergo Journal International 27, no. 3 (March 26, 2018): 79–96. http://dx.doi.org/10.1007/s40629-018-0056-0.

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Pusch, Emanuel, Harald Renz, and Chrysanthi Skevaki. "Respiratory virus-induced heterologous immunity." Allergo Journal 27, no. 3 (April 26, 2018): 28–45. http://dx.doi.org/10.1007/s15007-018-1580-4.

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8

Hussell, Tracy. "Heterologous immunity meets tissue-specific training." Nature Reviews Immunology 16, no. 5 (April 4, 2016): 275. http://dx.doi.org/10.1038/nri.2016.41.

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Agrawal, Babita, Shakti Singh, Nancy Gupta, Wen Li, Satish Vedi, and Rakesh Kumar. "Unsolved Puzzles Surrounding HCV Immunity: Heterologous Immunity Adds Another Dimension." International Journal of Molecular Sciences 18, no. 8 (July 27, 2017): 1626. http://dx.doi.org/10.3390/ijms18081626.

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10

Adams, Andrew B., Thomas C. Pearson, and Christian P. Larsen. "Heterologous immunity: an overlooked barrier to tolerance." Immunological Reviews 196, no. 1 (December 2003): 147–60. http://dx.doi.org/10.1046/j.1600-065x.2003.00082.x.

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11

Shah, Javeed A., Cecilia S. Lindestam Arlehamn, David J. Horne, Alessandro Sette, and Thomas R. Hawn. "Nontuberculous Mycobacteria and Heterologous Immunity to Tuberculosis." Journal of Infectious Diseases 220, no. 7 (June 4, 2019): 1091–98. http://dx.doi.org/10.1093/infdis/jiz285.

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AbstractDevelopment of an improved tuberculosis (TB) vaccine is a high worldwide public health priority. Bacillus Calmette-Guerin (BCG), the only licensed TB vaccine, provides variable efficacy against adult pulmonary TB, but why this protection varies is unclear. Humans are regularly exposed to non-tuberculous mycobacteria (NTM) that live in soil and water reservoirs and vary in different geographic regions around the world. Immunologic cross-reactivity may explain disparate outcomes of BCG vaccination and susceptibility to TB disease. Evidence supporting this hypothesis is increasing but challenging to obtain due to a lack of reliable research tools. In this review, we describe the progress and bottlenecks in research on NTM epidemiology, immunology and heterologous immunity to Mtb. With ongoing efforts to develop new vaccines for TB, understanding the effect of NTM on vaccine efficacy may be a critical determinant of success.
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12

Welsh, Raymond M., and Robert S. Fujinami. "Pathogenic epitopes, heterologous immunity and vaccine design." Nature Reviews Microbiology 5, no. 7 (July 2007): 555–63. http://dx.doi.org/10.1038/nrmicro1709.

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13

Moens, Leen, Greet Wuyts, Jan Verhaegen, and Xavier Bossuyt. "Cross-Protective Immunity against Heterologous Streptococcus pneumoniae." Infection and Immunity 80, no. 5 (April 12, 2012): 1944–45. http://dx.doi.org/10.1128/iai.06397-11.

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14

Gyssens, I. C., and M. G. Netea. "Heterologous effects of vaccination and trained immunity." Clinical Microbiology and Infection 25, no. 12 (December 2019): 1457–58. http://dx.doi.org/10.1016/j.cmi.2019.05.024.

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15

Lemckert, Angelique A. C., Shawn M. Sumida, Lennart Holterman, Ronald Vogels, Diana M. Truitt, Diana M. Lynch, Anjali Nanda, et al. "Immunogenicity of Heterologous Prime-Boost Regimens Involving Recombinant Adenovirus Serotype 11 (Ad11) and Ad35 Vaccine Vectors in the Presence of Anti-Ad5 Immunity." Journal of Virology 79, no. 15 (August 1, 2005): 9694–701. http://dx.doi.org/10.1128/jvi.79.15.9694-9701.2005.

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ABSTRACT The high prevalence of preexisting immunity to adenovirus serotype 5 (Ad5) in human populations will likely limit the immunogenicity and clinical utility of recombinant Ad5 (rAd5) vector-based vaccines for human immunodeficiency virus type 1 and other pathogens. A potential solution to this problem is to utilize rAd vaccine vectors derived from rare Ad serotypes such as Ad35 and Ad11. We have previously reported that rAd35 vectors were immunogenic in the presence of anti-Ad5 immunity, but the immunogenicity of heterologous rAd prime-boost regimens and the extent that cross-reactive anti-vector immunity may limit this approach have not been fully explored. Here we assess the immunogenicity of heterologous vaccine regimens involving rAd5, rAd35, and novel rAd11 vectors expressing simian immunodeficiency virus Gag in mice both with and without anti-Ad5 immunity. Heterologous rAd prime-boost regimens proved significantly more immunogenic than homologous regimens, as expected. Importantly, all regimens that included rAd5 were markedly suppressed by anti-Ad5 immunity. In contrast, rAd35-rAd11 and rAd11-rAd35 regimens elicited high-frequency immune responses both in the presence and in the absence of anti-Ad5 immunity, although we also detected clear cross-reactive Ad35/Ad11-specific humoral and cellular immune responses. Nevertheless, these data suggest the potential utility of heterologous rAd prime-boost vaccine regimens using vectors derived from rare human Ad serotypes.
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Braucher, Douglas R., Jamie N. Henningson, Crystal L. Loving, Amy L. Vincent, Eun Kim, Julia Steitz, Andrea A. Gambotto, and Marcus E. Kehrli. "Intranasal Vaccination with Replication-Defective Adenovirus Type 5 Encoding Influenza Virus Hemagglutinin Elicits Protective Immunity to Homologous Challenge and Partial Protection to Heterologous Challenge in Pigs." Clinical and Vaccine Immunology 19, no. 11 (August 29, 2012): 1722–29. http://dx.doi.org/10.1128/cvi.00315-12.

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ABSTRACTInfluenza A virus (IAV) is widely circulating in the swine population and causes significant economic losses. To combat IAV infection, the swine industry utilizes adjuvanted whole inactivated virus (WIV) vaccines, using a prime-boost strategy. These vaccines can provide sterilizing immunity toward homologous virus but often have limited efficacy against a heterologous infection. There is a need for vaccine platforms that induce mucosal and cell-mediated immunity that is cross-reactive to heterologous viruses and can be produced in a short time frame. Nonreplicating adenovirus 5 vector (Ad5) vaccines are one option, as they can be produced rapidly and given intranasally to induce local immunity. Thus, we compared the immunogenicity and efficacy of a single intranasal dose of an Ad5-vectored hemagglutinin (Ad5-HA) vaccine to those of a traditional intramuscular administration of WIV vaccine. Ad5-HA vaccination induced a mucosal IgA response toward homologous IAV and primed an antigen-specific gamma interferon (IFN-γ) response against both challenge viruses. The Ad5-HA vaccine provided protective immunity to homologous challenge and partial protection against heterologous challenge, unlike the WIV vaccine. Nasal shedding was significantly reduced and virus was cleared from the lung by day 5 postinfection following heterologous challenge of Ad5-HA-vaccinated pigs. However, the WIV-vaccinated pigs displayed vaccine-associated enhanced respiratory disease (VAERD) following heterologous challenge, characterized by enhanced macroscopic lung lesions. This study demonstrates that a single intranasal vaccination with an Ad5-HA construct can provide complete protection from homologous challenge and partial protection from heterologous challenge, as opposed to VAERD, which can occur with adjuvanted WIV vaccines.
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17

Gil, Anna, Laurie L. Kenney, Rabinarayan Mishra, Levi B. Watkin, Nuray Aslan, and Liisa K. Selin. "Vaccination and heterologous immunity: educating the immune system." Transactions of The Royal Society of Tropical Medicine and Hygiene 109, no. 1 (January 2015): 62–69. http://dx.doi.org/10.1093/trstmh/tru198.

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18

Selin, Liisa K., Michael A. Brehm, Sung-Kwon Kim, and Hong D. Chen. "Heterologous immunity and the CD8 T cell network." Springer Seminars in Immunopathology 24, no. 2 (November 1, 2002): 149–68. http://dx.doi.org/10.1007/s00281-002-0111-1.

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19

Shann, Frank. "Heterologous Immunity and the Nonspecific Effects of Vaccines." Pediatric Infectious Disease Journal 23, no. 6 (June 2004): 555–58. http://dx.doi.org/10.1097/01.inf.0000130155.42392.04.

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20

Messina, N. L., P. Zimmermann, and N. Curtis. "The impact of vaccines on heterologous adaptive immunity." Clinical Microbiology and Infection 25, no. 12 (December 2019): 1484–93. http://dx.doi.org/10.1016/j.cmi.2019.02.016.

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21

Mathur, Harsh, Paula M. O'Connor, Paul D. Cotter, Colin Hill, and R. Paul Ross. "Heterologous Expression of Thuricin CD Immunity Genes in Listeria monocytogenes." Antimicrobial Agents and Chemotherapy 58, no. 6 (April 7, 2014): 3421–28. http://dx.doi.org/10.1128/aac.00090-14.

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ABSTRACTBacteriocins are ribosomally synthesized peptides that can have a narrow or broad spectrum of antimicrobial activity. Bacteriocin producers typically possess dedicated immunity systems that often consist of an ATP-binding cassette (ABC) transporter system and/or a dedicated immunity protein. Here we investigated the genes responsible for immunity to thuricin CD, a narrow-spectrum two-peptide sactibiotic produced byBacillus thuringiensisDPC6431. Heterologous expression of putative thuricin CD immunity determinants allowed us to identify and investigate the relative importance of the individual genes and gene products that contribute to thuricin CD immunity. We established that TrnF and TrnG are the individual components of an ABC transporter system that provides immunity to thuricin CD. We also identified a hitherto overlooked open reading frame located upstream oftrnFpredicted to encode a 79-amino-acid transmembrane protein. We designated this newly discovered genetrnIand established that TrnI alone can provide protection against thuricin CD.
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22

Toptygina, A. P. "Heterologous immune responses in health and disease." Russian Journal of Infection and Immunity 10, no. 2 (May 22, 2020): 269–76. http://dx.doi.org/10.15789/2220-7619-hir-1292.

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Immunological memory and tolerance represent major achievements and advantages of adaptive immunity. Organisms bearing adaptive immunity display prominent competitive advantages in the fight against infections. Memory immune cells are preserved for decades and are able to repel a second attack of an infectious agent. However, studies performed in the XXI century have shown that even unrelated pathogens may be quickly and effectively destroyed by memory cells. This type of response is called heterologous so that heterologous immune response is mainly typical to viral infections and other intracellular infections, where T-cells play a lead role in protection. This review will discuss various mechanisms involved in implementing T-cell cross-reactivity, describe molecular prerequisites for heterologous T-cell responses. Experimental evidence of memory T-cell potential to heterologous immune response in mouse models and in human infections are also discussed. Heterologous immune response is an important immune arm in adults and the elderly when the yield of naive cells to the periphery declines due to thymus involution. Along with obvious advantages, heterologous immune response leads to imbalanced memory T-cell repertoire, replacement of immunodominant epitopes with minor ones allowing viruses to evade immune response that results in virus persistence, or, conversely, fulminant infection course. Another threat of heterologous immune response due to switch in dominant repertoire of recognizable epitopes is presented by random self-epitope recognition, which can lead to development of autoimmune pathology. Heterologous immunity can also disrupt drug-induced tolerance in organ and tissue transplants and lead to graft rejection. Heterologous immune response should be taken into consideration while developing and using new vaccines, especially in adults and the elderly.
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23

Roberts, Mark, Andrew Bacon, Jingli Li, and Steven Chatfield. "Prior Immunity to Homologous and HeterologousSalmonella Serotypes Suppresses Local and Systemic Anti-Fragment C Antibody Responses and Protection from Tetanus Toxin in Mice Immunized with Salmonella Strains Expressing Fragment C." Infection and Immunity 67, no. 8 (August 1, 1999): 3810–15. http://dx.doi.org/10.1128/iai.67.8.3810-3815.1999.

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ABSTRACT We have investigated the effect of preexisting immunity to homologous (Salmonella typhimurium) or heterologous (S. dublin) serotypes of Salmonella on the ability of an attenuated S. typhimurium aroA aroD vector (BRD509) to immunize mice against the heterologous antigen fragment C (FrgC). We studied two strains, BRD847 and BRD937, expressing FrgC carried on plasmids that differ only with respect to the promoter controlling FrgC expression, the nirB promoter in the case of BRD847 and the htrA promoter in the case of BRD937. Mice were preimmunized orally with S. typhimurium BRD509,S. dublin aroA aroD (BRD620), or saline. Forty-four days later, they were immunized orally with BRD847 or BRD937. Prior immunity to S. typhimurium severely depressed the serum immunoglobulin G (IgG) and IgA anti-FrgC response in both BRD847- and BRD937-immunized mice. Mice with existing immunity to S. dublin also had lower IgG anti-FrgC geometric mean titers (GMTs) than did mice preimmunized with saline, but this difference was significant only in the case of mice immunized with BRD937. However, in nonimmune mice or in mice preimmunized with S. typhimuriumor S. dublin, the anti-FrgC IgG GMTs were always higher in mice in the BRD937 groups than in the equivalent BRD847 groups. This is reflected in the effect of prior immunity on the ability of oral immunization with BRD847 or BRD937 to protect mice from challenge with a lethal dose of tetanus toxin. All of the mice preimmunized with saline and then immunized with BRD847 or BRD937 survived challenge. Only 20% of the animals immunized with BRD847 and 60% of the mice in the BRD937 group survived tetanus toxin challenge if they were preimmunized with BRD509. Preexisting immunity to S. dublindid not affect the ability of BRD937 to immunize mice against tetanus, but it did reduce the efficiency of BRD847: only 60% percent of the mice survived challenge. The intestinal secretory IgA responses to FrgC were very similar in the BRD847 and BRD937 groups. Prior immunity did depress the IgA anti-FrgC titers but only significantly so in the mice preimmunized with BRD509. These results show that preexistingSalmonella immunity, particularly to homologous serotypes, can severely compromise the ability of live Salmonellavectors to deliver heterologous antigens to the mammalian immune system. However, the results also indicate that this may be overcome by the design of more powerful in vivo expression systems.
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Cheesman, Sandra, Ahmed Raza, and Richard Carter. "Mixed Strain Infections and Strain-Specific Protective Immunity in the Rodent Malaria Parasite Plasmodium chabaudi chabaudi in Mice." Infection and Immunity 74, no. 5 (May 2006): 2996–3001. http://dx.doi.org/10.1128/iai.74.5.2996-3001.2006.

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ABSTRACT Important to malaria vaccine design is the phenomenon of “strain-specific” immunity. Using an accurate and sensitive assay of parasite genotype, real-time quantitative PCR, we have investigated protective immunity against mixed infections of genetically distinct cloned “strains” of the rodent malaria parasite Plasmodium chabaudi chabaudi in mice. Four strains of P. c. chabaudi, AS, AJ, AQ, and CB, were studied. One round of blood infection and drug cure with a single strain resulted in a partial reduction in parasitemia, compared with levels for naïve mice, in challenge infections with mixed inocula of the immunizing (homologous) strain and a heterologous strain. In all cases, the numbers of blood-stage parasites of each genotype were reduced to similar degrees. After a second, homologous round of infection and drug cure followed by challenge with homologous and heterologous strains, the parasitemias were reduced even further. In these circumstances, moreover, the homologous strain was reduced much faster than the heterologous strain in all of the combinations tested. That the immunity induced by a single infection did not show “strain specificity,” while the immunity following a second, homologous infection did, suggests that the “strain-specific” component of protective immunity in malaria may be dependent upon immune memory. The results show that strong, protective immunity induced by and effective against malaria parasites from a single parasite species has a significant “strain-specific” component and that this immunity operates differentially against genetically distinct parasites within the same infection.
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25

Selin, Liisa K., Myriam F. Wlodarczyk, Anke R. Kraft, Siwei Nie, Laurie L. Kenney, Roberto Puzone, and Franco Celada. "Heterologous immunity: Immunopathology, autoimmunity and protection during viral infections." Autoimmunity 44, no. 4 (January 20, 2011): 328–47. http://dx.doi.org/10.3109/08916934.2011.523277.

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26

Selin, Liisa K., Markus Cornberg, Michael A. Brehm, Sung-Kwon Kim, Claudia Calcagno, Dario Ghersi, Roberto Puzone, Franco Celada, and Raymond M. Welsh. "CD8 memory T cells: cross-reactivity and heterologous immunity." Seminars in Immunology 16, no. 5 (October 2004): 335–47. http://dx.doi.org/10.1016/j.smim.2004.08.014.

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27

Urbani, S., P. Fisicaro, B. Amadei, G. Missale, A. Bertoletti, and C. Ferrari. "26 Heterologous T cell immunity during severe HCV infection." Journal of Hepatology 40 (January 2004): 10. http://dx.doi.org/10.1016/s0168-8278(04)90026-8.

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28

Che, Jenny W., Liisa K. Selin, and Raymond M. Welsh. "Evaluation of non-reciprocal heterologous immunity between unrelated viruses." Virology 482 (August 2015): 89–97. http://dx.doi.org/10.1016/j.virol.2015.03.002.

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29

Diepolder, Helmut M. "Can Specific Heterologous Immunity Boost Hepatitis B Vaccine Responses?" Journal of Infectious Diseases 198, no. 3 (August 2008): 297–98. http://dx.doi.org/10.1086/589721.

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30

Chimalapati, Suneeta, Jonathan Cohen, and Jeremy S. Brown. "Reply to “Cross-Protective Immunity against Heterologous Streptococcus pneumoniae”." Infection and Immunity 80, no. 5 (April 12, 2012): 1946. http://dx.doi.org/10.1128/iai.00098-12.

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31

Sharma, Shalini, and Paul G. Thomas. "The two faces of heterologous immunity: protection or immunopathology." Journal of Leukocyte Biology 95, no. 3 (November 8, 2013): 405–16. http://dx.doi.org/10.1189/jlb.0713386.

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32

Adams, Andrew B., Matthew A. Williams, Thomas R. Jones, Nozomu Shirasugi, Megan M. Durham, Susan M. Kaech, E. John Wherry, et al. "Heterologous immunity provides a potent barrier to transplantation tolerance." Journal of Clinical Investigation 111, no. 12 (June 15, 2003): 1887–95. http://dx.doi.org/10.1172/jci200317477.

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33

Page, Kathleen R., Alan L. Scott, and Yukari C. Manabe. "The expanding realm of heterologous immunity: friend or foe?" Cellular Microbiology 8, no. 2 (February 2006): 185–96. http://dx.doi.org/10.1111/j.1462-5822.2005.00653.x.

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34

Taylor, Devon K., David Neujahr, and Laurence A. Turka. "Heterologous immunity and homeostatic proliferation as barriers to tolerance." Current Opinion in Immunology 16, no. 5 (October 2004): 558–64. http://dx.doi.org/10.1016/j.coi.2004.07.007.

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35

de Alencar, Bruna C. G., Pedro M. Persechini, Filipe A. Haolla, Gabriel de Oliveira, Jaline C. Silverio, Joseli Lannes-Vieira, Alexandre V. Machado, Ricardo T. Gazzinelli, Oscar Bruna-Romero, and Mauricio M. Rodrigues. "Perforin and Gamma Interferon Expression Are Required for CD4+ and CD8+ T-Cell-Dependent Protective Immunity against a Human Parasite, Trypanosoma cruzi, Elicited by Heterologous Plasmid DNA Prime-Recombinant Adenovirus 5 Boost Vaccination." Infection and Immunity 77, no. 10 (August 3, 2009): 4383–95. http://dx.doi.org/10.1128/iai.01459-08.

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ABSTRACT A heterologous prime-boost strategy using plasmid DNA, followed by replication-defective recombinant adenovirus 5, is being proposed as a powerful way to elicit CD4+ and CD8+ T-cell-mediated protective immunity against intracellular pathogens. We confirmed this concept and furthered existing research by providing evidence that the heterologous prime-boost regimen using the gene encoding amastigote surface protein 2 elicited CD4+ and CD8+ T-cell-mediated protective immunity (reduction of acute parasitemia and prolonged survival) against experimental infection with Trypanosoma cruzi. Protective immunity correlated with the presence of in vivo antigen-specific cytotoxic activity prior to challenge. Based on this, our second goal was to determine the outcome of infection after heterologous prime-boost immunization of perforin-deficient mice. These mice were highly susceptible to infection. A detailed analysis of the cell-mediated immune responses in immunized perforin-deficient mice showed an impaired gamma interferon (IFN-γ) secretion by immune spleen cells upon restimulation in vitro with soluble recombinant antigen. In spite of a normal numeric expansion, specific CD8+ T cells presented several functional defects detected in vivo (cytotoxicity) and in vitro (simultaneous expression of CD107a/IFN-γ or IFN-γ/tumor necrosis factor alpha) paralleled by a decreased expression of CD44 and KLRG-1. Our final goal was to determine the importance of IFN-γ in the presence of highly cytotoxic T cells. Vaccinated IFN-γ-deficient mice developed highly cytotoxic cells but failed to develop any protective immunity. Our study thus demonstrated a role for perforin and IFN-γ in a number of T-cell-mediated effector functions and in the antiparasitic immunity generated by a heterologous plasmid DNA prime-adenovirus boost vaccination strategy.
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36

Elliott, Salenna R., Rachel D. Kuns, and Michael F. Good. "Heterologous Immunity in the Absence of Variant-Specific Antibodies after Exposure to Subpatent Infection with Blood-Stage Malaria." Infection and Immunity 73, no. 4 (April 2005): 2478–85. http://dx.doi.org/10.1128/iai.73.4.2478-2485.2005.

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ABSTRACT We examined immunity induced by subpatent blood-stage malaria (undetectable by microscopy) using the rodent malaria parasite, Plasmodium chabaudi chabaudi, postulating that limited infection may allow expansion of antigen-specific T cells that are normally deleted by apoptosis. After three infections drug cured at 48 h, mice were protected against high-dose challenge with homologous or heterologous parasites (different strain or variant). Immunity differed from that generated by three untreated, patent infections. Subpatently infected mice lacked immunoglobulin G (IgG) to variant surface antigens, despite producing similar titers of total malaria-specific IgG to those produced by patently infected mice, including antibodies specific for merozoite surface antigens conserved between heterologous strains. Antigen-specific proliferation of splenocytes harvested prechallenge was significantly higher in subpatently infected mice than in patently infected or naive mice. In subpatently infected mice, lymphoproliferation was similar in response to homologous and heterologous parasites, suggesting that antigenic targets of cell-mediated immunity were conserved. A Th1 cytokine response was evident during challenge. Apoptosis of CD4+ and CD8+ splenic lymphocytes occurred during patent but not subpatent infection, suggesting a reason for the relative prominence of cell-mediated immunity after subpatent infection. In conclusion, subpatent infection with blood stage malaria parasites induced protective immunity, which differed from that induced by patent infection and targeted conserved antigens. These findings suggest that alternative vaccine strategies based on delivery of multiple parasite antigens at low dose may induce effective immunity targeting conserved determinants.
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37

Bekkering, Siroon, Jorge Domínguez-Andrés, Leo A. B. Joosten, Niels P. Riksen, and Mihai G. Netea. "Trained Immunity: Reprogramming Innate Immunity in Health and Disease." Annual Review of Immunology 39, no. 1 (April 26, 2021): 667–93. http://dx.doi.org/10.1146/annurev-immunol-102119-073855.

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Traditionally, the innate and adaptive immune systems are differentiated by their specificity and memory capacity. In recent years, however, this paradigm has shifted: Cells of the innate immune system appear to be able to gain memory characteristics after transient stimulation, resulting in an enhanced response upon secondary challenge. This phenomenon has been called trained immunity. Trained immunity is characterized by nonspecific increased responsiveness, mediated via extensive metabolic and epigenetic reprogramming. Trained immunity explains the heterologous effects of vaccines, which result in increased protection against secondary infections. However, in chronic inflammatory conditions, trained immunity can induce maladaptive effects and contribute to hyperinflammation and progression of cardiovascular disease, autoinflammatory syndromes, and neuroinflammation. In this review we summarize the current state of the field of trained immunity, its mechanisms, and its roles in both health and disease.
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38

Roy, Sreeja, Clare M. Williams, Julian Pardo, Danushka K. Wijesundara, and Yoichi Furuya. "Impact of Pre-Existing Immunity on Live Attenuated Influenza Vaccine-Induced Cross-Protective Immunity." Vaccines 8, no. 3 (August 20, 2020): 459. http://dx.doi.org/10.3390/vaccines8030459.

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The efficacy of the intranasally (i.n.) delivered live attenuated influenza vaccine (LAIV) is variable and, in some seasons, suboptimal. In this study, we report that LAIV exhibits cross-protective efficacy in mice, potentially associated with cellular immunity as opposed to antigen-specific antibody responses. However, pre-exposure to the intramuscularly (i.m.) delivered inactivated influenza vaccine (IIV) severely impaired LAIV-induced cross-protection against heterologous challenge, potentially by inhibiting replication of LAIV. Our findings suggest that pre-existing immunity afforded by IIV suppresses cross-protective T cell immunogenicity of LAIV.
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39

Thorner, Anna R., Angelique A. C. Lemckert, Jaap Goudsmit, Diana M. Lynch, Bonnie A. Ewald, Matthew Denholtz, Menzo J. E. Havenga, and Dan H. Barouch. "Immunogenicity of Heterologous Recombinant Adenovirus Prime-Boost Vaccine Regimens Is Enhanced by Circumventing Vector Cross-Reactivity." Journal of Virology 80, no. 24 (October 11, 2006): 12009–16. http://dx.doi.org/10.1128/jvi.01749-06.

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ABSTRACT The high prevalence of preexisting immunity to adenovirus serotype 5 (Ad5) in human populations has led to the development of recombinant adenovirus (rAd) vectors derived from rare Ad serotypes as vaccine candidates for human immunodeficiency virus type 1 and other pathogens. Vaccine vectors have been constructed from Ad subgroup B, including rAd11 and rAd35, as well as from Ad subgroup D, including rAd49. However, the optimal combination of vectors for heterologous rAd prime-boost vaccine regimens and the extent of cross-reactive vector-specific neutralizing antibodies (NAbs) remain poorly defined. We have shown previously that the closely related vectors rAd11 and rAd35 elicited low levels of cross-reactive NAbs. Here we show that these cross-reactive NAbs correlated with substantial sequence homology in the hexon hypervariable regions (HVRs) and suppressed the immunogenicity of heterologous rAd prime-boost regimens. In contrast, vectors with lower hexon HVR homology, such as rAd35 and rAd49, did not elicit detectable cross-reactive vector-specific NAbs. Consistent with these findings, rAd35-rAd49 vaccine regimens proved more immunogenic than both rAd35-rAd5 and rAd35-rAd11 regimens in mice with anti-Ad5 immunity. These data suggest that optimal heterologous rAd prime-boost regimens should include two vectors that are both rare in human populations to circumvent preexisting antivector immunity as well as sufficiently immunologically distinct to avoid cross-reactive antivector immunity.
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Penarete-Vargas, Diana Marcela, Marie Noelle Mévélec, Sarah Dion, Edouard Sèche, Isabelle Dimier-Poisson, and Thierry Fandeur. "Protection against Lethal Neospora caninum Infection in Mice Induced by Heterologous Vaccination with a mic1 mic3 Knockout Toxoplasma gondii Strain." Infection and Immunity 78, no. 2 (December 7, 2009): 651–60. http://dx.doi.org/10.1128/iai.00703-09.

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ABSTRACT Neospora caninum and Toxoplasma gondii are closely related, obligate intracellular parasites infecting a wide range of vertebrate hosts and causing abortion and neonatal morbidity and mortality. Several lines of evidence suggest that cross immunity between these two pathogens could be exploited in the design of strategies for heterologous vaccination. We assessed the ability of an attenuated strain of T. gondii (“mic1-3KO strain”) conferring strong protection against chronic and congenital toxoplasmosis to protect mice against lethal N. caninum infection. Mice immunized with mic1-3KO tachyzoites by the oral and intraperitoneal routes developed a strong cellular Th1 response and displayed significant protection against lethal heterologous N. caninum infection, with survival rates of 70% and 80%, respectively, whereas only 30% of the nonimmunized mice survived. We report here the acquisition of heterologous protective immunity against N. caninum following immunization with a live attenuated mic1-3KO strain of T. gondii.
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41

Stojanovic, Marijana, Ivana Lukic, Emilija Marinkovic, Ana Kovacevic, Radmila Miljkovic, Joshua Tobias, Irma Schabussova, et al. "Cross-Reactive Effects of Vaccines: Heterologous Immunity between Tetanus and Chlamydia." Vaccines 8, no. 4 (December 1, 2020): 719. http://dx.doi.org/10.3390/vaccines8040719.

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Vaccines can have heterologous effects on the immune system, i.e., effects other than triggering an immune response against the disease targeted by the vaccine. We investigated whether monoclonal antibodies (mAbs) specific for tetanus could cross-react with Chlamydia and confer heterologous protection against chlamydial infection. The capability of two tetanus-specific mAbs, namely mAb26 and mAb51, to prevent chlamydial infection has been assessed: (i) in vitro, by performing a neutralization assay using human conjunctival epithelial (HCjE) cells infected with Chlamydia trachomatis serovar B, and (ii) in vivo, by using a guinea pig model of Chlamydiacaviae-induced inclusion conjunctivitis. The mAb26 has been superior in comparison with mAb51 in the prevention of chlamydial infection in HCjE cells. The mAb26 has conferred ≈40% inhibition of the infection, compared to less than 5% inhibition in the presence of the mAb51. In vivo, mAb26 significantly diminished ocular pathology intensity in guinea pigs infected with C. caviae compared to either the mAb51-treated or sham-treated guinea pigs. Our data provide insights that tetanus immunization generates antibodies which induce heterologous chlamydial immunity and promote protection beyond the intended target pathogen.
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42

van den Hoogen, Bernadette G., Sander Herfst, Miranda de Graaf, Leo Sprong, Rob van Lavieren, Geert van Amerongen, Selma Yüksel, Ron A. M. Fouchier, Albert D. M. E. Osterhaus, and Rik L. de Swart. "Experimental infection of macaques with human metapneumovirus induces transient protective immunity." Journal of General Virology 88, no. 4 (April 1, 2007): 1251–59. http://dx.doi.org/10.1099/vir.0.82663-0.

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Human metapneumovirus (hMPV), a member of the family Paramyxoviridae, is a causative agent of acute respiratory-tract illness. Two main hMPV lineages circulate worldwide and reinfections occur frequently. It is unclear what level of protection is induced by natural hMPV infection, what the durability of this protection is and whether it differs for reinfection with homologous or heterologous viruses. Here, protective immunity in cynomolgus macaques at different time points after inoculation with molecularly cloned prototype viruses of the two main lineages of hMPV has been addressed. Animals received a homologous challenge at 4, 6 or 12 weeks after the primary infection. In addition, animals that had been inoculated three times within 10 weeks were challenged with homologous or heterologous virus 8 months later. Primary infection with 107 TCID50 resulted in virus shedding and induction of virus-neutralizing antibody responses, with higher titres against the homologous than the heterologous virus. Infections associated with virus shedding and seroconversion protected completely from homologous reinfection within 6 weeks, and partly at 12 weeks, after primary infection. Eight months later, protection had waned to virtually undetectable levels. This study demonstrates that experimental hMPV infection induces transient protective immunity.
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43

Calcagno, Claudia, Roberto Puzone, Yanthe E. Pearson, Yiming Cheng, Dario Ghersi, Liisa K. Selin, Raymond M. Welsh, and Franco Celada. "Computer simulations of heterologous immunity: Highlights of an interdisciplinary cooperation." Autoimmunity 44, no. 4 (January 27, 2011): 304–14. http://dx.doi.org/10.3109/08916934.2010.523220.

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44

Krummey, Scott M., Ryan J. Martinez, Rakieb Andargachew, Danya Liu, Maylene Wagener, Jacob E. Kohlmeier, Brian D. Evavold, Christian P. Larsen, and Mandy L. Ford. "Low-Affinity Memory CD8+ T Cells Mediate Robust Heterologous Immunity." Journal of Immunology 196, no. 6 (February 10, 2016): 2838–46. http://dx.doi.org/10.4049/jimmunol.1500639.

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45

Manlove, Luke S., Jason M. Schenkel, Kezia R. Manlove, Kristen E. Pauken, Richard T. Williams, Vaiva Vezys, and Michael A. Farrar. "Heterologous Vaccination and Checkpoint Blockade Synergize To Induce Antileukemia Immunity." Journal of Immunology 196, no. 11 (April 25, 2016): 4793–804. http://dx.doi.org/10.4049/jimmunol.1600130.

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46

Butkeviciute, Egle, Christine E. Jones, and Steven G. Smith. "Heterologous effects of infant BCG vaccination: potential mechanisms of immunity." Future Microbiology 13, no. 10 (August 2018): 1193–208. http://dx.doi.org/10.2217/fmb-2018-0026.

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47

Daniels, Keith A., Steven D. Hatfield, Raymond M. Welsh, and Michael A. Brehm. "MHC basis of T cell-dependent heterologous immunity to arenaviruses." Virology 464-465 (September 2014): 213–17. http://dx.doi.org/10.1016/j.virol.2014.07.012.

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48

Urbani, Simona, Barbara Amadei, Paola Fisicaro, Massimo Pilli, Gabriele Missale, Antonio Bertoletti, and Carlo Ferrari. "Heterologous T cell immunity in severe hepatitis C virus infection." Journal of Experimental Medicine 201, no. 5 (March 7, 2005): 675–80. http://dx.doi.org/10.1084/jem.20041058.

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Hepatitis C virus (HCV) can cause liver disease of variable severity. Expansion of preexisting memory CD8 T cells by cross-reactivity with a new heterologous virus infection has been shown in mice to shape the repertoire of the primary response and to influence virus-related immunopathology (Selin, L.K. 2004. Immunity. 20:5–16). To determine whether this mechanism can influence the course of HCV infection, we analyzed the features of the HCV-specific CD8 T cell response in eight patients with acute HCV infection, two of whom had a particularly severe illness. Patients with severe hepatitis, but not those with mild disease, showed an extremely vigorous CD8 T cell response narrowly focused on a single epitope (NS3 1073–1081), which cross-reacted with an influenza neuraminidase sequence. Our results suggest that CD8 T cell cross-reactivity influences the severity of the HCV-associated liver pathology and depicts a model of disease induction that may apply to different viral infections.
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49

Kleinnijenhuis, J., R. van Crevel, and M. G. Netea. "Trained immunity: consequences for the heterologous effects of BCG vaccination." Transactions of the Royal Society of Tropical Medicine and Hygiene 109, no. 1 (January 1, 2015): 29–35. http://dx.doi.org/10.1093/trstmh/tru168.

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50

Thirumalapura, Nagaraja R., Emily C. Crossley, David H. Walker, and Nahed Ismail. "Persistent Infection Contributes to Heterologous Protective Immunity against Fatal Ehrlichiosis." Infection and Immunity 77, no. 12 (October 5, 2009): 5682–89. http://dx.doi.org/10.1128/iai.00720-09.

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ABSTRACT Human monocytotropic ehrlichiosis (HME), an emerging and often life-threatening tick-transmitted disease, is caused by the obligately intracellular bacterium Ehrlichia chaffeensis. HME is modeled in C57BL/6 mice using Ehrlichia muris, which causes persistent infection, and Ixodes ovatus Ehrlichia (IOE), which is either acutely lethal or sublethal depending on the dose and route of inoculation. A persistent primary E. muris infection, but not a sublethal IOE infection, protects mice against an ordinarily lethal secondary IOE challenge. In the present study, we determined the role of persistent infection in maintenance of protective memory immune responses. E. muris-infected mice were treated with doxycycline or left untreated and then challenged with an ordinarily lethal dose of IOE. Compared to E. muris-primed mice treated with doxycycline, untreated mice persistently infected with E. muris had significantly greater numbers of antigen-specific gamma interferon-producing splenic memory T cells, significant expansion of CD4+ CD25+ T regulatory cells, and production of transforming growth factor β1 in the spleen. Importantly, E. muris-primed mice treated with doxycycline showed significantly greater susceptibility to challenge infection with IOE compared to untreated mice persistently infected with E. muris. The study indicated that persistent ehrlichial infection contributes to heterologous protection by stimulating the maintenance of memory T-cell responses.
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