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-Induced Class II Transactivator Expression by a 19-kDa Lipoprotein from Mycobacterium tuberculosis: A Potential Mechanism for Immune Evasion1
* Department of Pathology,
Division of Infectious Diseases and
Tuberculosis Research Unit, Case Western Reserve University and University of Hospitals of Cleveland, Cleveland, OH 44106; and Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195
Mycobacterium tuberculosis (MTB) persists inside macrophages despite vigorous immune responses. MTB and MTB 19-kDa lipoprotein inhibit class II MHC (MHC-II) expression and Ag processing by a Toll-like receptor 2-dependent mechanism that is shown in this study to involve a defect in IFN-
induction of class II transactivator (CIITA). Exposure of macrophages to MTB or MTB 19-kDa lipoprotein inhibited IFN--induced MHC-II expression, but not IL-4-induced MHC-II expression, by preventing induction of mRNA for CIITA (total, type I, and type IV), IFN regulatory factor-1, and MHC-II. MTB 19-kDa lipoprotein induced mRNA for suppressor of cytokine signaling (SOCS)1 but did not inhibit IFN--induced Stat1 phosphorylation. Furthermore, the lipoprotein inhibited MHC-II Ag processing in SOCS1-/- macrophages. MTB 19-kDa lipoprotein did not inhibit translocation of phosphorylated Stat1 to the nucleus or Stat1 binding to and transactivation of IFN--sensitive promoter constructs. Thus, MTB 19-kDa lipoprotein inhibited IFN- signaling independent of SOCS1 and without interfering with the activation of Stat1. Inhibition of IFN--induced CIITA by MTB 19-kDa lipoprotein may allow MTB to evade detection by CD4+ T cells.
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