Both myeloid (e.g., macrophages and monocytes, and DCs) and non myeloid cells (e.g., keratinocytes and epithelial cells) are shown to sense certain "danger" signals and activate inflammasome, thus resulting in secretion of proinflammatory cytokines (e.g., IL-1b and IL-18). However, it is not clear whether lymphocyes can activate certain inflammasomes or not.
The present knowledge is at a point where inflammasome are large intracellular multiprotein complexes that cause apoptosis in Lymphocytes in sepsis. As you have rightly mentioned, Dr D Chaubey, the answer to your question is still in infancy I feel.
A difficult question for most of us, however I wish people following inflammation/immunity in health and sickness follow this and see if they can help answer this question, or guide scientists to certain lead.
Regards to all.
Prof. Divaker Choubey,
This is a very interesting question. Our group focus on B cells and we found B cells can sense certain "danger" signals and can be activated non-typically. Maybe some published papers have already found similar phenomenons. I'll share a published paper and hope more researchers share their ideas!
It was initially assumed that inflammasomes are contained to innate immune cells. However, after their non-immunological functions, people have shown their expression and functions in T cells. (Pubmed ID: 17164409 ; 31379813; 19717512 ; 25539818 ; PMC4835240).
B cells can process antigen and present antigen also owing to partial APC properties. It is not surprising that inflammasome has been reported in B cells. Dr. Eva has shown that glucan and CpG induced NLRP3 activation in B cells.
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