Lack of skin test reactivity to common mycobacterial antigens in human immunodeficiency virus infected individuals with high CD4 counts.

Abstract

Background -T cell response to mycobacterial antigens may be directed against those antigens common to all mycobacteria (group i), those restricted to slow (group ii) or fast growers (group iii), or those which are species-or subspeciesspecific (group iv). These responses were assessed by skin testing patients infected with the human immunodeficiency virus (HIV) and healthy controls with reagents derived from different strains ofmycobacteria. Methods -Skin test responses to new tuberculins prepared from Mycobacterium tuberculosis, M avium serotypes 4 and 8, and either M intracellulare or M flavescens antigens were evaluated prospectively in 51 HIV infected patients and 67 healthy controls.Results -Assessment of induration at 72 hours showed absence of skin test response to common mycobacterial antigens in all 27 HIV positive patients with CD4 counts of > 400/mm3 (range 400-1594, median 540) compared with 27% reactivity in controls; complete anergy was demonstrated in 24 patients with CD4 counts of < 400/mm3. By contrast, no difference in species or subspecies-specific responses was found between healthy controls and HIV positive patients with CD4 counts of ¢ 400/mm3. Conclusions -Subsets of CD4 + T helper cells are instrumental in determining the balance between cell-mediated and humoral immunity. One T helper subset (TH1) produces cytokines that increase cellular immunity and is stimulated by group i common mycobacterial antigens. Lack of this response, but preservation of responses to species-specific antigens while CD4 counts are near normal, may indicate an early failing of THI immunity and explain the increased susceptibility of HIV positive patients to mycobacterial infection early on in the evolution of their HIV infection. (Thorax 1996;51:932-935)

Psoriasis patients have T-cells with reduced responsiveness to common mycobacterial antigens

“…In diseases with a basis of altered immunity, responsiveness to group i, common mycobacterial antigens may be lost. This has been shown for tuberculosis [14] and multibacillary leprosy [15], for rheumatoid arthritis (RA) [16], early in HIV infection [17] and in persons in the silent seropositive phase of infection with Trypanosoma cruzi [18]. Our results (here, and [8]) show that the same may be true for psoriasis, though it is important to realise that this alone does not prove that mycobacteria cause the disease.…”

Dietary linoleic acid, immune inhibition and disease

“…Tuberculosis is strongly associated with the diminished type 1 response24 and depressed CD4+ count characteristic of HIV infection,25 and has been noted to occur at a higher CD4+ count than most other opportunistic infections 26. This may be due to the early loss of Th1 immunity reported in HIV infection at a stage when CD4+ counts are near-normal 27. Multi-drug-resistant tuberculosis is associated with a poor Th1 response 28…”

Correlation of the lung microbiota with metabolic profiles in bronchoalveolar lavage fluid in HIV infection

“…Further, fatty acid metabolism in addition to glycerophospholipid and linoleate metabolic pathways also correlated with the lung microbial species in these HIV-infected individuals; these have previously been shown to be altered systemically in HIV-infected individuals [ 18 ]. High dietary linoleic acid can lead to excessive prostaglandin-E2 production, which can depress cellular immunity specifically associated with the Th1 subset of T cells, which is also reduced in HIV infection [ 19 , 20 ]. Alterations in surfactant glycerophospholipid have been seen in AIDS patients with acute Pneumocystis pneumonia [ 21 ].…”