• Graeme Meintjes, Katalin Andrea Wilkinson, Molebogeng Xheeda Rangaka, Keira Skolimowska, Kerryn van Veen, Musaed Abrahams, Ronnett Seldon, Dominique J Pepper, Kevin Rebe, Priscilla Mouton, Gilles van Cutsem, Mark Patrick Nicol, Gary Maartens, and Robert John Wilkinson.
• F.R.C.P., Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa. r.j.wilkinson@imperial.ac.uk.
• Am. J. Respir. Crit. Care Med. 2008 Nov 15; 178 (10): 1083-9.

RationaleTuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) induced by combination antiretroviral therapy (cART) has been attributed to dysregulated expansion of tuberculin PPD-specific IFN-gamma-secreting CD4(+) T cells.ObjectivesTo investigate the role of type 1 helper T cell expansions and regulatory T cells in HIV-TB IRIS.MethodsLongitudinal and cross-sectional studies of Mycobacterium tuberculosis-specific IFN-gamma enzyme-linked immunospot responses and flow cytometric analysis of blood cells from a total of 129 adults with HIV-1-associated tuberculosis, 98 of whom were prescribed cART.Measurements And Main ResultsIn cross-sectional analysis the frequency of IFN-gamma-secreting T cells recognizing early secretory antigenic target (ESAT)-6, alpha-crystallins 1 and 2, and PPD of M. tuberculosis was higher in patients with TB-IRIS than in similar patients treated for both HIV-1 and tuberculosis who did not develop IRIS (non-IRIS; P ConclusionsThere is an association between helper T-cell type 1 expansions and TB-IRIS, but the occurrence of similar expansions in non-IRIS brings into question whether these are causal. The defect in immune regulation responsible for TB-IRIS remains to be fully elucidated.

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