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1

Leonard, Patricia, and Sanjiv Sur. "Interleukin-12." BioDrugs 17, no. 1 (2003): 1–7. http://dx.doi.org/10.2165/00063030-200317010-00001.

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&NA;. "Interleukin-12." Inpharma Weekly &NA;, no. 1124 (February 1998): 7. http://dx.doi.org/10.2165/00128413-199811240-00013.

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Trinchieri, Giorgio. "Interleukin-12." Clinical Immunotherapeutics 3, no. 4 (April 1995): 262–70. http://dx.doi.org/10.1007/bf03259278.

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Clinton, Steven K., Eduardo Canto, and Michael A. O'Donnell. "INTERLEUKIN-12." Urologic Clinics of North America 27, no. 1 (February 2000): 147–55. http://dx.doi.org/10.1016/s0094-0143(05)70242-1.

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Weiner, David. "Plasmid Interleukin 12." AIDS 14, no. 12 (August 2000): 1759–60. http://dx.doi.org/10.1097/00002030-200008180-00010.

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Leng, S. X., and J. A. Elias. "Interleukin-11 inhibits macrophage interleukin-12 production." Journal of Immunology 159, no. 5 (September 1, 1997): 2161–68. http://dx.doi.org/10.4049/jimmunol.159.5.2161.

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Abstract IL-12 is a heterodimeric cytokine produced by phagocytic and other cells with important physiologic and pathologic properties. Regulated IL-12 production is crucial for the generation of protective Th1 responses to infectious agents. In contrast, IL-12 excess contributes to the pathogenesis of a variety of autoimmune and inflammatory disorders. To further understand the processes regulating IL-12 production, we determined whether IL-11 regulated monocyte/macrophage production of this cytokine moiety. IL-11 did not alter the IL-12 (p70) production of unstimulated THP-1 monocytic cells or human blood monocytes. It did, however, inhibit, in a dose-dependent fashion, the IL-12 production of IFN-gamma plus Staphylococcus aureus Cowan strain 1-stimulated THP-1 cells and stimulated blood monocytes. This inhibition of IL-12 protein production was associated with a proportionate decrease in IL-12 p35 and p40 mRNA accumulation. Nuclear run-on assays revealed comparable decreases in IL-12 p35 and p40 gene transcription. IL-11 did not similarly regulate monocyte/macrophage production of IL-8 or macrophage inflammatory protein-1alpha (MIP-1alpha) and IL-6 did not similarly inhibit IL-12 elaboration. These studies demonstrate that IL-11 is a potent inhibitor of monocyte/macrophage IL-12 production and that this inhibitory effect is, at least in part, transcriptionally mediated. They also demonstrate that this inhibition is not the result of a generalized suppression of macrophage effector function and that the ability to inhibit monocyte/macrophage IL-12 production is not a generalized property of all IL-6-type cytokines.
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Fox, Robert J., and Abdolmohamad M. Rostami. "Anti???Interleukin-12 Antibody." BioDrugs 13, no. 4 (April 2000): 233–41. http://dx.doi.org/10.2165/00063030-200013040-00002.

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&NA;. "Interleukin-12 trial halted." Reactions Weekly &NA;, no. 556 (June 1995): 2. http://dx.doi.org/10.2165/00128415-199505560-00003.

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&NA;. "Interleukin-12 studies continue." Reactions Weekly &NA;, no. 558 (July 1995): 2. http://dx.doi.org/10.2165/00128415-199505580-00003.

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&NA;. "Interleukin-12 trial halted." Inpharma Weekly &NA;, no. 992 (June 1995): 21. http://dx.doi.org/10.2165/00128413-199509920-00047.

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&NA;. "Interleukin-12 studies continue." Inpharma Weekly &NA;, no. 994 (July 1995): 21. http://dx.doi.org/10.2165/00128413-199509940-00042.

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KATIYAR, S. "Interleukin-12 and photocarcinogenesis." Toxicology and Applied Pharmacology 224, no. 3 (November 1, 2007): 220–27. http://dx.doi.org/10.1016/j.taap.2006.11.017.

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Maguire, H. C. "INTERLEUKIN 12 AS IMMUNOADJUVANT." Journal of Immunotherapy 16, no. 3 (October 1994): 240. http://dx.doi.org/10.1097/00002371-199410000-00032.

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de Rie, M. A. "Interleukin 12 and Psoriasis." Dermatology 199, no. 2 (1999): 101. http://dx.doi.org/10.1159/000018213.

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Trinchieri, Giorgio, and Franca Gerosa. "Immunoregulation by interleukin-12." Journal of Leukocyte Biology 59, no. 4 (April 1996): 505–11. http://dx.doi.org/10.1002/jlb.59.4.505.

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Ma, X., A. D'Andrea, M. Kubin, M. Aste-Amezaga, A. Sartori, J. Monteiro, L. Showe, M. Wysocka, and G. Trinchieri. "Production of interleukin-12." Research in Immunology 146, no. 7-8 (September 1995): 432–38. http://dx.doi.org/10.1016/0923-2494(96)83012-4.

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Crutcher, J. M., M. M. Stevenson, M. Sedegah, and S. L. Hoffman. "Interleukin-12 and malaria." Research in Immunology 146, no. 7-8 (September 1995): 552–59. http://dx.doi.org/10.1016/0923-2494(96)83031-8.

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Tsai, I. San, Chi-Cheng Tsai, Ya-Ping Ho, Kun-Yen Ho, Yi-Min Wu, and Chun-Cheng Hung. "Interleukin-12 and interleukin-16 in periodontal disease." Cytokine 31, no. 1 (July 2005): 34–40. http://dx.doi.org/10.1016/j.cyto.2005.02.007.

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BACON, CHRIS M., SARAH S. CHO, and JOHN J. O'SHEA. "Signal Transduction by Interleukin-12 and Interleukin-2." Annals of the New York Academy of Sciences 795, no. 1 Interleukin 1 (October 1996): 41–59. http://dx.doi.org/10.1111/j.1749-6632.1996.tb52654.x.

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Torti, Dorothea C., and Steven R. Feldman. "Interleukin-12, interleukin-23, and psoriasis: Current prospects." Journal of the American Academy of Dermatology 57, no. 6 (December 2007): 1059–68. http://dx.doi.org/10.1016/j.jaad.2007.07.016.

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Sánchez, E., S. Morales, L. Paco, M. A. López-Nevot, C. Hidalgo, J. Jiménez-Alonso, B. Torres, et al. "Interleukin 12 (IL12B), interleukin 12 receptor (IL12RB1) and interleukin 23 (IL23A) gene polymorphism in systemic lupus erythematosus." Rheumatology 44, no. 9 (May 31, 2005): 1136–39. http://dx.doi.org/10.1093/rheumatology/keh697.

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Orozco, Gisela, Miguel A. González-Gay, Laura Paco, Miguel A. López-Nevot, Manuel Guzmán, Dora Pascual-Salcedo, Alejandro Balsa, and Javier Martín. "Interleukin 12 (IL12B) and Interleukin 12 Receptor (IL12RB1) Gene Polymorphisms in Rheumatoid Arthritis." Human Immunology 66, no. 6 (June 2005): 710–14. http://dx.doi.org/10.1016/j.humimm.2005.02.004.

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Mattner, Frank, Susanne Fischer, Stefanie Guckes, Shenchu Jin, Hildegard Kaulen, Edgar Schmitt, Erwin Rüde, and Tieno Germann. "The interleukin-12 subunit p40 specifically inhibits effects of the interleukin-12 heterodimer." European Journal of Immunology 23, no. 9 (September 1993): 2202–8. http://dx.doi.org/10.1002/eji.1830230923.

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Eman, Arif Rahman, Vitayani Muchtar Sri, Tabri Farida, Wahab Siswanto, Adriani Anni, Seweng Arifin, and Sjahril Rizalinda. "EVALUATION OF INTERLEUKIN-12 AND INTERLEUKIN-4 LEVELS IN MULTIBACILLARY-TYPE LEPROSY PATIENT 12 MONTHS AFTER RIFAMPICIN OFLOXACIN MINOCYCLINE COMBINATION THERAPY." International Journal of Medical Reviews and Case Reports 2, no. 4 (May 3, 2018): 161–65. https://doi.org/10.5455/IJMRCR.MULTIBACILLARY-TYPE-LEPROSY-INTERLEUKINS.

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Background: Leprosy is a chronic infectious disease caused by Mycobacterium leprae. In leprosy, cell-mediated immune responses are an important aspect of host resistance to mycobacterial infections and allegedly governed by anequilibrium between type 1 cytokines including Interleukin-12 (IL-12); with type 2 cytokines such as Interleukin-4 (IL-4). Currently, the World Health Organization (WHO) recommends 3 leprosy treatment regimens, one of them is Rifampicin Ofloxacin Minocycline (ROM). To date, studies on the effects of ROM on leprosy have been limited, none have specifically assessed the effects of ROM on specific immune systems, especially cytokines. Methods: The study was conducted by prospective research method. The sample of this research were all multibacillary (MB) type of leprosy patients according to WHO classification who had received ROM therapy and recorded as the patient at research location and had medical record previous of interleukin-12 and interleukin-4 levels. After 12 months of ROM therapy, blood samples were collected and calculated using the Enzyme-Linked Immunosorbent Assay (ELISA) using the Quantikine® high sensitivity (HSv) kit. Results: There was a statistically significant increase in IL-4 after 12 months of a 3-months-ROM therapy. In contrast, the levels of IL-12 after 12 months showed significant decreases. Conclusions: Increased levels of IL-4 and decreased IL-12 can be caused by many factors. Therefore, further research with a closer supervision is required.
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Lu, Zhiyu, Keye Xu, Xiaoying Wang, Yan Li, and Mingcai Li. "Interleukin 39: a new member of interleukin 12 family." Central European Journal of Immunology 45, no. 2 (2020): 214–17. http://dx.doi.org/10.5114/ceji.2020.97911.

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Rentzos, M., C. Nikolaou, E. Andreadou, G. P. Paraskevas, A. Rombos, M. Zoga, A. Tsoutsou, F. Boufidou, E. Kapaki, and D. Vassilopoulos. "Circulating interleukin-10 and interleukin-12 in Parkinson’s disease." Acta Neurologica Scandinavica 119, no. 5 (May 2009): 332–37. http://dx.doi.org/10.1111/j.1600-0404.2008.01103.x.

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Tahara, H., L. Zitvogel, W. J. Storkus, T. G. McKinney, P. D. Robbins, and M. T. Lotze. "CANCER GENE THERAPY USING INTERLEUKIN-12 (IL-12)." Journal of Immunotherapy 16, no. 3 (October 1994): 245. http://dx.doi.org/10.1097/00002371-199410000-00053.

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&NA;. "Interleukin-12 toxicity mystery solved." Reactions Weekly &NA;, no. 580 (December 1995): 2. http://dx.doi.org/10.2165/00128415-199505800-00002.

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&NA;. "Interleukin-12 toxicity mystery solved." Inpharma Weekly &NA;, no. 1016 (December 1995): 21. http://dx.doi.org/10.2165/00128413-199510160-00046.

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Romani, L., P. Puccetti, and F. Bistoni. "Interleukin-12 in infectious diseases." Clinical Microbiology Reviews 10, no. 4 (October 1997): 611–36. http://dx.doi.org/10.1128/cmr.10.4.611.

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Interleukin-12 (IL-12) is a potent immunoregulatory cytokine that is crucially involved in a wide range of infectious diseases. In several experimental models of bacterial, parasitic, viral, and fungal infection, endogenous IL-12 is required for early control of infection and for generation and perhaps maintenance of acquired protective immunity, directed by T helper type 1 (Th1) cells and mediated by phagocytes. Although the relative roles of IL-12 and gamma interferon in Th1-cell priming may be to a significant extent pathogen dependent, common to most infections is that IL-12 regulates the magnitude of the gamma interferon response at the initiation of infection, thus potentiating natural resistance, favoring Th1-cell development; and inhibiting Th2 responses. Treatment of animals with IL-12, either alone or as a vaccine adjuvant, has been shown to prevent disease by many of the same infectious agents, by stimulating innate resistance or promoting specific reactivity. Although IL-12 may enhance protective memory responses in vaccination or in combination with antimicrobial chemotherapy, it is yet unclear whether exogenous IL-12 can alter established responses in humans. Continued investigation into the possible application of IL-12 therapy to human infections is warranted by the role of the cytokine in inflammation, immunopathology, and autoimmunity.
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Romani, L., P. Puccetti, and F. Bistoni. "Interleukin-12 in infectious diseases." Clinical microbiology reviews 10, no. 4 (1997): 611–36. http://dx.doi.org/10.1128/cmr.10.4.611-636.1997.

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Bashyam, Hema. "Interleukin-12: A master regulator." Journal of Experimental Medicine 204, no. 5 (May 7, 2007): 969. http://dx.doi.org/10.1084/jem.2045fta.

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Early resistance to pathogens requires a swift response from NK cells. In 1989, Giorgio Trinchieri identified an NK growth factor and activator, later called interleukin-12 (IL-12). This discovery helped reveal the regulatory link between innate and adaptive immunity.
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Adorini, Luciano. "Interleukin 12 and autoimmune diabetes." Nature Genetics 27, no. 2 (February 2001): 131–32. http://dx.doi.org/10.1038/84732.

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Bubeník, Jan. "Interleukin 12 in Cancer Treatment." Folia Biologica 57, no. 1 (2011): 1–2. http://dx.doi.org/10.14712/fb2011057010001.

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Interleukin 12 (IL-12) is made up of two disulphidelinked chains, p35 and p40. The cytokine is produced by monocytes, macrophages, myeloid dendritic cells and B cells. It stimulates development of NK cells and TH1 differentiation of CD4+ T cells, thus participating in the regulation of the immune response (for a review, see Klein and Hořejší, 1997; Grufman and Kärre, 2000; Jinushi and Tahara, 2009). Recently, the structurally similar but functionally different cytokine IL-23 displaying anti-tumour effects and related to the IL-12 family of cytokines was discovered (Engel and Neurath, 2010). In a variety of experimental tumour models it has been demonstrated that tumour immunogenicity could be enhanced by administration of IL-12 or by gene therapy employing insertion of the IL12 gene into tumour cells (for a review, see Bubeník, 1996; Bubeník et al., 2000; Bubeník, 2008). IL-12 is known to activate IFN-γ production by NK and T cells and development of cytotoxic T lymphocytes in vitro (Grufman and Kärre, 2000; Dranhoff, 2004; Indrova et al., 2008, 2009). IL-12 was also found to have anti-angiogenic activity, apparently through the induction of IFN-γ-inducible protein 10 (Sgadari et al., 1996). Each of these properties of IL-12 may contribute to the anti-tumour activity (Tsung et al., 1998). However, serious toxicity has been associated with the IL-12 systemic administration. Therefore, peritumoral administration of IL-12, expression of the IL12 genes in the peritumoral milieu after injection of IL12 gene-modified vaccines, or nanoparticle-based gene delivery (Hallaj-Nezhadi et al., 2010) were considered to help avoid the systemic toxicity. It has also been shown that the IL12 gene-modified cellular vaccines augment the efficacy of cancer surgery and chemotherapy in experimental models mimicking some human tumours (Indrová et al., 2006, 2008; Malvicini et al. 2009; Bubeník and Šímová, 2009). With regard to the mechanism of these IL-12 effects, it was reported that IL-12 is an indispensable cytokine for activating dendritic cells (Jinushi and Tahara, 2009). It stimulates dendritic cellmediated cross-presentation of tumour-associated antigens and promotes the TH1 differentiation crucial for tumour defence mechanisms (Engleman 2003; Dranhoff, 2004). The administration of DNA encoding human IL-12 by intratumoral injection into patients with metastatic melanoma (Heinzerling et al., 2005), intratumoral injection of a recombinant canarypox virus expressing IL-12 (Triozzi et al., 2005), IL-12 plasmid electroporation (Daud et al., 2008), IL12 gene therapy by peritumoral injection of IL-12-transduced autologous fibroblasts (Kang et al., 2001), vaccination with IL12 gene-modified autologous melanoma cells (Sun et al., 1998), utilization of IL-12 plasmid/lipopolymer complexes for the treatment of recurrent ovarian cancer (Anwer et al., 2010), treatment of multiple myeloma by subcutaneous IL-12 injections (Lacy et al., 2009), as well as other procedures (for a review see Jinushi and Tahara, 2009) were found to induce local immune responses, to enhance cellular and humoral immune reactions, as well as to prolong survival of patients and to decrease tumour neoangiogenesis. Taken together, preclinical studies as well as phase I–III clinical trials have clearly demonstrated that local IL-12 therapy and peritumoral administration of the IL-12-based tumour vaccines can induce and enhance tumour immunity and by this way prolong survival of the tumour-bearing individuals. In addition, utilization of the IL-12-based therapeutic procedures as adjuvant treatment together with conventional therapeutic modalities, chemotherapy and surgery also provided promising results. However, many technical problems have still to be solved (Berrando et al., 2009) and the translational therapeutic trials have to be carefully evaluated before the definitive conclusions regarding the actual therapeutic potency of this novel and promising strategies for the management of cancer patients can be drawn and relevant therapeutic protocols can be designed.
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Sacks, G. P., D. Scott, H. Tivnann, T. Mire-Sluis, I. L. Sargent, and C. W. G. Redman. "Interleukin-12 and pre-eclampsia." Journal of Reproductive Immunology 34, no. 2 (September 1997): 155–58. http://dx.doi.org/10.1016/s0165-0378(97)00028-4.

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Bryan, Dani-Louise, Joanna S. Hawkes, and Robert A. Gibson. "Interleukin-12 in Human Milk." Pediatric Research 45, no. 6 (June 1999): 858–59. http://dx.doi.org/10.1203/00006450-199906000-00013.

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Sturmhoefel, K., K. Lee, M. O. Toole, H. M. Swiniarski, A. J. Dorner, and S. F. Wolf(xc*). "Interleukin 12 as vaccine adjuvant." Research in Immunology 149, no. 1 (January 1998): 37–39. http://dx.doi.org/10.1016/s0923-2494(98)80041-2.

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Rowe, PaulM. "Cautious optimism over interleukin-12." Lancet 345, no. 8962 (June 1995): 1432. http://dx.doi.org/10.1016/s0140-6736(95)92618-6.

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Trinchieri, Giorgio, Manthrasalam Rengaraju, Annalisa D'Andrea, Nicholas M. Valiante, Marek Kubin, Miguel Aste, and Jihed Chehimi. "Producer cells of interleukin-12." Immunology Today 14, no. 5 (May 1993): 237–38. http://dx.doi.org/10.1016/0167-5699(93)90173-i.

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MA, XIAOJING, MIGUEL ASTE-AMEZAGA, and GIORGIO TRINCHIERI. "Regulation of Interleukin-12 Production." Annals of the New York Academy of Sciences 795, no. 1 Interleukin 1 (October 1996): 13–25. http://dx.doi.org/10.1111/j.1749-6632.1996.tb52651.x.

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BLISS, JUDY, RICHARD MAYLOR, KEYA STOKES, KRISTIN S. MURRAY, MARA A. KETCHUM, and STANLEY F. WOLF. "Interleukin-12 as Vaccine Adjuvant." Annals of the New York Academy of Sciences 795, no. 1 Interleukin 1 (October 1996): 26–35. http://dx.doi.org/10.1111/j.1749-6632.1996.tb52652.x.

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Podlaski, Frank J., Venkata B. Nanduri, Jeffrey D. Hulmes, Yu-Ching E. Pan, Wayne Levin, Waleed Danho, Richard Chizzonite, Maurice K. Gately, and Alvin S. Stern. "Molecular characterization of interleukin 12." Archives of Biochemistry and Biophysics 294, no. 1 (April 1992): 230–37. http://dx.doi.org/10.1016/0003-9861(92)90162-p.

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Trinchieri, Giorgio, Manthrasalam Rengaraju, Annalisa D'Andrea, Nicholas M. Valiante, Marek Kubin, Miguel Aste, and Jihed Chehimi. "Producer cells of interleukin 12." Parasitology Today 9, no. 3 (March 1993): 97. http://dx.doi.org/10.1016/0169-4758(93)90215-2.

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Brunda, Michael J., and Maurice K. Gately. "Antitumor Activity of Interleukin-12." Clinical Immunology and Immunopathology 71, no. 3 (June 1994): 253–55. http://dx.doi.org/10.1006/clin.1994.1081.

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Karp, Christopher L. "Interleukin-12: Amiss in MS." Annals of Neurology 45, no. 6 (June 1999): 689–92. http://dx.doi.org/10.1002/1531-8249(199906)45:6<689::aid-ana1>3.0.co;2-m.

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Gately, Maurice K., Louis M. Renzetti, Jeanne Magram, Alvin S. Stern, Luciano Adorini, Ueli Gubler, and David H. Presky. "THE INTERLEUKIN-12/INTERLEUKIN-12-RECEPTOR SYSTEM: Role in Normal and Pathologic Immune Responses." Annual Review of Immunology 16, no. 1 (April 1998): 495–521. http://dx.doi.org/10.1146/annurev.immunol.16.1.495.

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Wang, Xin, Victoria L. Wilkinson, Frank J. Podlaski, Chang-you Wu, Alvin S. Stern, David H. Presky, and Jeanne Magram. "Characterization of mouse interleukin-12 p40 homodimer binding to the interleukin-12 receptor subunits." European Journal of Immunology 29, no. 6 (June 1999): 2007–13. http://dx.doi.org/10.1002/(sici)1521-4141(199906)29:06<2007::aid-immu2007>3.0.co;2-0.

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Yücel, Özlem Özer, Ezel Berker, Semra Gariboğlu та Harika Otlu. "Interleukin-11, interleukin-1β, interleukin-12 and the pathogenesis of inflammatory periodontal diseases". Journal of Clinical Periodontology 35, № 5 (травень 2008): 365–70. http://dx.doi.org/10.1111/j.1600-051x.2008.01212.x.

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GATELY, MAURICE K., DAISY M. CARVAJAL, SUZANNE E. CONNAUGHTON, SILKE GILLESSEN, RAJEEV R. WARRIER, KENNETH D. KOLINSKY, VICTORIA L. WILKINSON, et al. "Interleukin-12 Antagonist Activity of Mouse Interleukin-12 p40 Homodimer in Vitro and in Vivo." Annals of the New York Academy of Sciences 795, no. 1 Interleukin 1 (October 1996): 1–12. http://dx.doi.org/10.1111/j.1749-6632.1996.tb52650.x.

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Robinson, Cory M., and Gerard J. Nau. "Interleukin‐12 and Interleukin‐27 Regulate Macrophage Control ofMycobacterium tuberculosis." Journal of Infectious Diseases 198, no. 3 (August 2008): 359–66. http://dx.doi.org/10.1086/589774.

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