Sertoli cells, can function as non-professional tolerogenic antigen-presenting cells, and sustain the blood-testis barrier formed by their tight junctions. The NOD-like receptor family members and the @entity5704 inflammasome play a key role in pro-inflammatory innate immunity signalling pathways. Limited data exist on @entity18506 and @entity6820 expression in @entity1 and @entity19 Sertoli cells. Currently, there is no data on inflammasome expression or function in Sertoli cells. We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, @entity2939 \ @entity18506 and @entity6820 crosstalk converged in NFkB activation and elicited a @entity5704 activation, leading to de novo synthesis and inflammasome priming. This led to @entity9302 activation and @entity1356 secretion. We demonstrated this process was controlled by mechanisms linked to autophagy. @entity18506 promoted @entity1356 restriction and autophagosome maturation arrest, while @entity6820 promoted @entity9302 activation, @entity1356 secretion and autophagy maturation. @entity5704 modulated @entity18506 and @entity1356 expression, while @entity6820 inversely promoted @entity1356 . This study is proof of concept that Sertoli cells, upon specific stimulation, could participate in @entity4810 pathogenesis via inflammatory cytokine induction.

Sertoli cells have a functional XXXX inflammasome that can modulate autophagy and cytokine production.

@entity1 :: ('9606', 'Species') :: ['human'] @entity4810 :: ('MESH:D007248', 'Disease') :: ['male infertility'] @entity5704 :: ('114548', 'Gene') :: ['NALP3'] @entity19 :: ('10090', 'Species') :: ['mouse'] @entity9302 :: ('834', 'Gene') :: ['caspase-1'] @entity1356 :: ('3553', 'Gene') :: ['IL-1b', 'pro-IL-1b'] @entity6820 :: ('64127', 'Gene') :: ['NOD2'] @entity2939 :: ('7099', 'Gene') :: ['TLR4'] @entity18506 :: ('10392', 'Gene') :: ['NOD1']
@entity5704 :: (114548,Gene) :: ['NALP3']
