Document 0670
 DOCN  M9650670
 TI    Dysregulated production of interleukin-10 (IL-10) and IL-12 by
       peripheral blood lymphocytes from human immunodeficiency virus-infected
       individuals is associated with altered proliferative responses to recall
       antigens.
 DT    9605
 AU    Daftarian MP; Diaz-Mitoma F; Creery WD; Cameron W; Kumar A; Department
       of Pediatrics, Children's Hospital of Eastern Ontario,; University of
       Ottawa, Canada.
 SO    Clin Diagn Lab Immunol. 1995 Nov;2(6):712-8. Unique Identifier :
       AIDSLINE MED/96157376
 AB    The loss of immune function following infection with human
       immunodeficiency virus (HIV) may result from altered production of
       immunoregulatory cytokines such as interleukin-10 (IL-10) and IL-12. In
       this study, we analyzed IL-10 and IL-12 production by mitogen-stimulated
       peripheral blood mononuclear cells (PBMC) from HIV+ individuals and
       correlated their levels with proliferative responses to the recall
       antigens HIV p25 and influenza virus. We report two distinct groups of
       HIV+ patients. One group produced small amounts of IL-10, had PBMC that
       proliferated in response to recall antigens, and demonstrated enhanced
       recall antigen-induced proliferation upon addition of anti-IL-10
       antibodies and/or IL-12. Conversely, the second group produced high
       levels of IL-10, had PBMC that failed to proliferate to recall antigens,
       and did not demonstrate enhanced proliferation upon addition of
       anti-IL-10 antibodies and/or IL-12. Mitogen-stimulated PBMC from both
       groups produced significantly lower levels of IL-12 than did those from
       HIV- controls. Analysis of the source of the IL-10-producing cell subset
       in PBMC demonstrated that in HIV+ individuals, IL-10 is produced by
       monocytes, while in HIV- controls, it is produced by both T cells and
       monocytes. Taken together, our results suggest that monocytes from HIV+
       individuals secrete decreased amounts of IL-12, a Th1-type cytokine,
       which may lead to the development of Th2-type responses characterized by
       high IL-10 secretion and immune dysfunction.
 DE    Acquired Immunodeficiency Syndrome/*IMMUNOLOGY/METABOLISM  Adult
       Antigens, Viral/IMMUNOLOGY  Cell Division/IMMUNOLOGY  Human  HIV
       Antigens/METABOLISM  Immunologic Memory  Interleukin-10/*BIOSYNTHESIS
       Interleukin-12/*BIOSYNTHESIS  Leukocytes, Mononuclear/*METABOLISM
       Lymphocyte Transformation/IMMUNOLOGY  Mitogens/PHARMACOLOGY
       Phytohemagglutinins/PHARMACOLOGY  Support, Non-U.S. Gov't
       T-Lymphocytes/*METABOLISM  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).