Immunology of tuberculosis.

Tuberculosis is a major health problem throughout the world causing large number of deaths, more than that from any other single infectious disease. The review attempts to summarize the information available on host immune response to Mycobacterium tuberculosis. Since the main route of entry of the causative agent is the respiratory route, alveolar macrophages are the important cell types, which combat the pathogen. Various aspects of macrophage-mycobacterium interactions and the role of macrophage in host response such as binding of M. tuberculosis to macrophages via surface receptors, phagosome-lysosome fusion, mycobacterial growth inhibition/killing through free radical based mechanisms such as reactive oxygen and nitrogen intermediates; cytokine-mediated mechanisms; recruitment of accessory immune cells for local inflammatory response and presentation of antigens to T cells for development of acquired immunity have been described. The role of macrophage apoptosis in containing the growth of the bacilli is also discussed. The role of other components of innate immune response such as natural resistance associated macrophage protein (Nramp), neutrophils, and natural killer cells has been discussed. The specific acquired immune response through CD4 T cells, mainly responsible for protective Th1 cytokines and through CD8 cells bringing about cytotoxicity, also has been described. The role of CD-1 restricted CD8(+) T cells and non-MHC restricted gamma/deltaT cells has been described although it is incompletely understood at the present time. Humoral immune response is seen though not implicated in protection. The value of cytokine therapy has also been reviewed. Influence of the host human leucocyte antigens (HLA) on the susceptibility to disease is discussed. Mycobacteria are endowed with mechanisms through which they can evade the onslaught of host defense response. These mechanisms are discussed including diminishing the ability of antigen presenting cells to present antigens to CD4(+) T cells; production of suppressive cytokines; escape from fused phagosomes and inducing T cell apoptosis. The review brings out the complexity of the host-pathogen interaction and underlines the importance of identifying the mechanisms involved in protection, in order to design vaccine strategies and find out surrogate markers to be measured as in vitro correlate of protective immunity.

Age-related changes in blood lymphocyte subsets of south Indian children.

BACKGROUND: Enumeration of lymphocyte subsets has been widely used for the diagnosis and monitoring of several haematological and immunological disorders. Various studies have demonstrated age, sex and racial differences in lymphocyte subset expression. Reference values are not available for Indian children and there is a need for this information to replace commonly used, but inappropriate, adult lymphocyte subset ranges. METHODS: One hundred thirty-eight healthy children between 3 and 15 years of age, attending a local government school in Chennai, South India were Included in the study. Haemoglobin levels, and total and differential cell counts were determined using an automated counter and lymphocyte subsets were analysed by flowcytometry. RESULTS: The mean (SD) absolute lymphocyte count declined with age from 4338 (1031) at 3 years to reach a plateau of 3096 (914) at 11-13 years (p < 0.05). A significant decline was also observed in the absolute numbers of CD3+, CD4+, CD8+ and CD19+ cells. However, the percentage values of CD3+, CD4+, CD8+, CD16/56+ cells and the CD4/CD8 ratio remained fairly stable across the age range. CONCLUSION: Our data would prove useful in interpreting disease-related changes in lymphocyte subsets in Indian children of different age groups. Age-related decrease in the absolute lymphocyte count as well as numbers of CD4 and CD8 cells was found to occur between the ages of 3 and 11 years. A normogram relating age to CD4 count has been developed.

Humoral immune response to filarial antigens in chyluria.

Humoral immune parameters like total immunoglobulins and specific antibody levels in serum were studied in filarial chyluria patients. Mean serum IgG was significantly reduced in this group compared to normal controls, while IgA and IgM levels remained comparable to controls. Anti-filarial antibody titre as measured by enzyme-linked immunosorbent assay also was significantly reduced. However, the total and specific IgE antibody titre was similar to that of controls. Specific IgE contents of the patients' sera could be related to their microfilaraemic status.