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Juzar Ali

Publications and source records attributed to Juzar Ali.

3 recordsLinked to original sources

Decreased expression of CD3zeta and nuclear transcription factor kappa B in patients with pulmonary tuberculosis: potential mechanisms and reversibility with treatment.

BACKGROUND: The protective immune response against Mycobacterium tuberculosis relies both on antigen-presenting cells and on T lymphocytes. In patients with different forms of tuberculosis, varying degrees of T cell function--ranging from positive delayed-type hypersensitivity, in asymptomatic infected healthy individuals, to the absence of the response, in patients with miliary or pulmonary tuberculosis (PTB)--have been reported. The decreased expression of CD3zeta reported in T cells from patients with either cancer or leprosy has provided possible explanations for the altered immune response observed in these diseases. METHODS: The present study aimed to compare the expression of CD3zeta , nuclear transcription factor- kappa B (NF- kappa B), arginase activity, and cytokine production in 20 patients with PTB, in 20 tuberculin-positive asymptomatic subjects, and in 14 tuberculin-negative control subjects. RESULTS: Compared with those in tuberculin (purified protein derivative)-negative control subjects, peripheral-blood T lymphocytes from patients with active PTB had significantly (P < .001) decreased expression of CD3zeta and absence of the p65/p50 heterodimer of NF- kappa B. These alterations were reversed only in patients who responded to treatment. Also reported here for the first time is that the presence of arginase activity in peripheral-blood mononuclear-cell lysates of patients with PTB parallels high production of interleukin-10. CONCLUSIONS: The presence of arginase could, in part, explain the decreased expression of CD3zeta . These findings provide a novel mechanism that may explain the T cell dysfunction observed in patients with PTB.

Adult↗

Mycobacterium avium complex pulmonary disease in immunocompetent patients.

Mycobacterium avium complex is becoming increasingly recognized as one of the most common mycobacterial pathogens in humans. It is rapidly becoming a significant cause of pulmonary disease even in those with an intact immunity. In 1997, the American Thoracic Society published recommendations for the diagnosis and treatment of nontuberculous mycobacteria. On the basis of the authors' clinical experience of the myriad presentations of pulmonary Mycobacterium avium complex disease in an immunocompetent host, a clinical classification is proposed. The current data are summarized, and a practical approach to management of the various pulmonary forms of the disease is provided.

Alveolitis, Extrinsic Allergic↗

Immunity against mycobacteria.

Mycobacterium tuberculosis is the most prevalent infectious pathogen in the world, largely due to its unique interactions with the human immune system. Even in a normal host, a frequent outcome of infection with M. tuberculosis is failure to completely eradicate the organisms, despite the development of cell-mediated immunity. Viable organisms persist in a state in which they do not progressively replicate, leading to latent infection, which carries a risk of breakdown into active (reactivation) tuberculosis at some point later in life. Key features of the immune response against mycobacteria are reviewed here, and potential mechanisms by which the organisms may subvert these host defenses are discussed. Despite the multicellular nature of the host response to infecting mycobacteria, the organisms cannot be eradicated and contribute to the ongoing worldwide epidemic with tuberculosis.

Journal Article↗