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The immunological response in pulmonary and pleural tuberculosis has been extensively studied. However, the response in tuberculous meningitis has not been well documented.1 In pulmonary disease, exposure to tuberculous antigens results in a T cell and natural killer cellular response, elaborating various cytokines, mainly of T helper type 1 (Th1) origin. Stimulated macrophages elaborate tumour necrosis factor (TNF) α, interleukin (IL) 12, and IL 1, promoting further recruitment and activation of macrophages and lymphocytes.
TNF α correlates with disease severity and may contribute to tissue necrosis; however, TNFα has also contributed to survival in mouse studies.2 Transforming growth factor β (Th3 cytokine) suppresses macrophage activation. IL 2 may be beneficial in promoting an immune response in HIV seropositive patients. Th1 and Th2 cytokine responses have been observed in cerebrospinal fluid (CSF) of HIV seronegative patients with tuberculous meningitis.3,4. Whether the response is similar in HIV seropositive patients with tuberculous meningitis is unknown.
We studied the cytokine response and its correlation with disease severity in HIV seropositive and HIV seronegative patients with tuberculous meningitis.
Tuberculous meningitis was diagnosed on clinical and CSF examination after exclusion of viral, acute bacterial, and other causes of aseptic meningitis. Disease severity was assessed according to …
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