Document 3219
 DOCN  M94A3219
 TI    Modulation of Th1 responses in HIV infection and tuberculosis (TB).
 DT    9412
 AU    Barnes P; Zhang M; Jones B; Univ. of Southern California, Los Angeles.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):126 (abstract no. PA0122). Unique
       Identifier : AIDSLINE ICA10/94369356
 AB    To evaluate the Th1/Th2 cytokine profile in HIV-infected TB patients, we
       evaluated proliferative responses to M. tb and patterns of cytokine
       production by PBMC from 40 TB patients, with or without concomitant HIV
       infection. Upon stimulation with M. tb in vitro, PBMC from HIV-infected
       TB patients had reduced proliferation (mean delta cpm 1989 versus 26110,
       p < 0.0001) and production of IFN-gamma (mean 822 versus 2278 pg/ml, p =
       0.004), but IL-10 production was not diminished (mean 711 versus 578
       pg/ml). We next used RT-PCR with internal controls to quantitate
       cytokine mRNA in M. tb-stimulated PBMC from TB patients, 12 with and 13
       without HIV infection. Samples were normalized to contain 0.4 attoM of
       CD3 delta chain cDNA, then amplified by PCR with cytokine-specific
       primers. mRNA for the Th1 cytokines IFN-gamma and IL-2 was significantly
       reduced in HIV-infected TB patients (mean .069 versus .544 attoM of
       IFN-gamma cDNA, and .003 versus .025 attoM of IL-2 cDNA). In contrast,
       mRNA for the Th2 cytokines IL-4 and IL-10 was comparable in TB patients
       with or without HIV infection. In purified CD4+ cells, mRNA for Th1
       cytokines was still lower in HIV-infected patients. M. tb-induced
       proliferative responses by PBMC from HIV-infected TB patients were
       markedly enhanced by addition of anti-IL-10 in 10/11 patients, and by
       addition of recombinant IL-12 in 6/10 patients. Proliferation was not
       enhanced by anti-IL-4. M. tb-induced production of IFN-gamma was
       markedly enhanced by anti-IL-10 or IL-12. We conclude that Th1 responses
       are reduced in HIV-infected TB patients, and that these responses can be
       augmented by antibodies to IL-10 or by IL-12.
 DE    Antibodies/PHARMACOLOGY  AIDS-Related Opportunistic
       Infections/*IMMUNOLOGY  Cells, Cultured  Comparative Study
       Cytokines/*BIOSYNTHESIS  DNA Primers  Human  Interferon Type
       II/BIOSYNTHESIS  Interleukin-10/ANTAGONISTS & INHIB/BIOSYNTHESIS
       Interleukin-2/BIOSYNTHESIS  Interleukin-4/ANTAGONISTS & INHIB
       Interleukins/PHARMACOLOGY  Lymphocyte Transformation/DRUG EFFECTS
       Lymphocytes/DRUG EFFECTS/*IMMUNOLOGY  Polymerase Chain Reaction
       Recombinant Proteins/PHARMACOLOGY  RNA, Messenger/BIOSYNTHESIS
       Tuberculosis/*IMMUNOLOGY  MEETING ABSTRACT

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