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NLRC3, a member of the NLR family, has been reported as a negative regulator of inflammatory signaling pathways in innate immune cells. However, the direct role of NLRC3 in modulation of CD4 +  T-cell responses in infectious diseases has not been studied. In the present study, we showed that NLRC3 plays an intrinsic role by suppressing the CD4 +  T cell phenotype in lung and spleen, including differentiation, activation, and proliferation. NLRC3 deficiency in CD4 +  T cells enhanced the protective immune response against  Mycobacterium tuberculosis  infection. Finally, we demonstrated that NLRC3 deficiency promoted the activation, proliferation, and cytokine production of CD4 +  T cells via negatively regulating the NF-κB and MEK-ERK signaling pathways. This study reveals a critical role of NLRC3 as a direct regulator of the adaptive immune response and its protective effects on immunity during  M .  tuberculosis  infection. Our findings also suggested that NLRC3 serves as a potential target for therapeutic intervention against tuberculosis.

NLRC3 negatively regulates CD4+ T cells and impacts protective immunity during Mycobacterium tuberculosis infection