To evaluate the relationship between the clinical presentation of tuberculosis and the CD4 cell count in patients with human immunodeficiency virus (HIV) infection, we evaluated clinical and laboratory features of 97 HIV-infected patients with tuberculosis in whom CD4 cell counts were available. Extrapulmonary tuberculosis was found in 30 (70%) of 43 patients with < or = 100 CD4 cells/microL, 10 (50%) of 20 patients with 101 to 200 CD4 cells/microL, seven (44%) of 16 patients with 201 to 300 CD4 cells/microL, and five (28%) of 18 patients with > 300 CD4 cells/microL (p = 0.02). Mycobacteremia was found in 18 (49%) of 37 patients with < or = 100 CD4 cells/microL, three (20%) of 15 patients with 101 to 200 CD4 cells/microL, one (7%) of 15 patients with 201 to 300 CD4 cells/microL, and none of eight patients with > 300 CD4 cells/microL (p = 0.002). Acid-fast smears were more often positive in patients with low CD4 cell counts. Positive tuberculin skin tests were more common in patients with high CD4 counts. On chest roentgenograms, mediastinal adenopathy was noted in 20 (34%) of 58 patients with < or = 200 CD4 cells/microL and four (14%) of 29 patients with > 200 CD4 cells/microL (p = 0.04). Pleural effusions were noted in six (10%) of 58 patients with < or = 200 CD4 cells/microL and eight (28%) of 29 patients with > 200 CD4 cells/microL (p = 0.04). The CD8 cell counts did not correlate with the manifestations of tuberculosis.(ABSTRACT TRUNCATED AT 250 WORDS)

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The clinical forms of leprosy constitute a spectrum that correlates closely with the degree of cellmediated immunity. Patients with tuberculoid leprosy develop strong cell-mediated responses and have only a few, localized lesions, whereas patients with multibacillary lepromatous leprosy are specifically unresponsive to antigens of Myobacterium leprae. T cells of the CD4+ subset predominate in tuberculoid lesions, whereas CD8+ cells predominate in lepromatous lesions. Monoclonal antibodies that distinguish subpopulations of CD4+ and CD8+ cells were used to analyze the distribution of T cells infiltrating lesions across the disease spectrum. In lepromatous lesions, T cells of T-suppressor phenotype (9.3-) were the predominant CD8+ cells and suppressor/inducer cells (2H4+, Leu-8+) represented half of the CD4+ subset. In tuberculoid lesions, helper T cells (CD4+4B4+) outnumbered suppressor/inducer T cells by 14:1, compared with a ratio of 1.2:1 in peripheral blood. Analysis of the precursor frequency of antigen-reactive T cells permitted us to estimate that there was a 100-fold enrichment of T cells able to proliferate in response to M. leprae antigens in tuberculoid lesions (2/100), when compared with blood from the same patients. The methods used here to characterize the T-lymphocyte subsets and frequency of antigen-reactive T cells in leprosy may be useful in analyzing imunological reactions occurring in lesions of other inflammatory and autoimmune diseases.There are at least two compelling reasons to study leprosy. The disease itself, affecting 10-15 million people worldwide, poses a significant health and economic burden on thirdworld countries. Second, because leprosy is a spectral disease in which pathology and immunology are inextricably related, it provides a unique critical model for investigating immunoregulatory mechanisms in humans.Leprosy is not a single critical entity but rather comprises a spectrum of clinical manifestations that correlate remarkably well with immunological responses to the organism (1). Patients with tuberculoid leprosy have a few localized lesions with rare organisms and a strong cell-mediated immune response directed against Myobacterium leprae antigens that ultimately kills and clears the bacilli, although often with concomitant injury to nerves. In contrast, lepromatous leprosy patients have numerous skin lesions containing extraordinarily high numbers of acid-fast bacilli and show specific immunological unresponsiveness to antigens of M. leprae in vivo and in vitro.The selective mechanisms of accumulation of lymphocytes, their antigen specificity, and immunological functions in inflammatory lesions of human infectious or autoimmune diseases remain largely unknown. Since the focal point of the immune response to M. leprae is the tissue granuloma, consisting of a collection of lymphocytes and macrophages, some of these questions can be approached directly through the study of cells infiltrating the lesions across the spectrum of leprosy.Immunohistological studies using m...

Leprosy provides a useful model for understanding immunoregulatory mechanisms in man. The disease forms a spectrum in which the immunologic response of the patient correlates with the clinical and histopathologic classification (1-3). At one end of the spectrum, patients with tuberculoid leprosy have one or several skin lesions in which bacilli can rarely be identified . CD4+ T lymphocytes predominate in these lesions (4-7) and respond to Mycobacterium leßrae in vitro (8). At the other end of the spectrum, patients with lepromatous leprosy have diffuse infiltration of skin and nerves with bacilli-laden macrophages. CD8+ cells predominate in lepromatous lesions and function as antigen-specific Ts cells in vitro (9, 10). The CD4+ lymphocytes derived from these lesions are unresponsive to M. leßrae . Imposed upon this spectrum are the so-called "reactional states" of reversal reaction and erythema nodosum leprosum (ENL)' that are of immunologic interest in understanding mechanisms of immunoregulation in man.The reversal reaction syndrome is associated with a marked rise in lymphocyte transformation to M. leßrae antigens in vitro, and is therefore thought to be a delayedtype hypersensitivity (DTH) reaction against M. leßrae antigens (11)(12)(13)(14)(15). Clinically, the condition is often associated with reduction or elimination of bacilli in lesions and sometimes followed by upgrading of the clinical and histological classification toward the tuberculoid pole. The pathogenesis of ENL reactions is somewhat controversial, thought to be due to immune complex deposition in the lesions (16-18) and/or increases in cell-mediated immunity (19,20).