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Memory immunity to Mycobacterium tuberculosis is independent of TLR2 signaling
Author(s) -
McBride Amanda B,
Potian Julius A,
Bhatt Kamlesh,
Salgame Padmini
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.553
Subject(s) - tlr2 , memory t cell , immunology , priming (agriculture) , immunity , biology , mycobacterium tuberculosis , immune system , cytokine , t cell , innate immune system , tuberculosis , medicine , pathology , botany , germination
High incidences of reinfection in endemic regions, as well as murine models of immunological memory, indicate that memory immunity to Mtb yields only short‐term protection. Antigen load, costimulation, or cytokine mileu during stimulation of naïve T cells may all factor into the development of memory T cells. Our laboratory has demonstrated that Mtb signaling via TLR2 leads to production of immunosuppressive cytokines, IL‐10 and IL‐6, by antigen presenting cells. We hypothesize that release of these cytokines during naïve T cell priming may limit memory T cell development. Therefore, in this study we investigated whether removal of TLR2 signaling would result in improved memory T cell response. Using a memory immunity model, the response of TLR2−/− mice following a secondary exposure to Mtb was compared to that of wild type mice based on assessment of bacterial burden, determination of the frequency of Mtb‐specific IFN‐γ producing cells, and phenotypic characterization of memory cells. Contrary to our prediction, our results indicate that the memory recall response in the absence of TLR2 is equivalent to that in wild type mice, suggesting that TLR2 does not impact memory induction. However, future studies will examine if TLR2 signaling negatively impacts the granulomatous response in the lung. This work was supported by grant A1071844 to PS.