Fig. 1
Innate immunity. a Innate immunity and novel MADS recognition. The classical innate immune system provides immediate and non-specific defense against pathogen or injury-generated molecules via PAMP/DAMP+PRR recognition in phagocytes and TC. Super Ag, a subset of pathogen toxins, can also bind to a multitude of TCR leading to TC activation. In addition, we propose a novel MADS recognition pathway, which allows metabolic risk factors to activate the innate immunity via responsive metabolic sensors in phagocytes and TC. The activation of innate immunity leads to pathogen elimination and inflammation (APC formation, cytokine generation, and TC activation). b Evidences of innate immunity in TC. Stimuli such as PAMP/DAMP, inflammatory cytokines and super Ag activate different subsets of TC and stimulate TC proliferation, inflammatory cytokine production, and phagocytosis. Words in red emphasize our newly proposed recognition pattern. Abbreviations: APC antigen present cell; Ag antigen; Ab antibody; BC B cell; BCR B cell receptor; CpG C, a cytosine triphosphate deoxynucleotide; p phosphodiester; G a guanine triphosphate deoxynucleotide; CTL cytotoxic T lymphocytes; DAMP danger-associated molecular patterns; d days; Foxp3 forkhead box P3; h hours; IL interleukin; IFN interferon; LPS lipopolysaccharide; MHC major histocompatibility complex; MADS metabolism-associated danger signal; NLR NOD (nucleotide-binding and oligomerization domain)-like receptors; PAMP pathogen-associated molecular patterns; PRR pattern recognition receptor; Poly(I:C) polyinosinic-polycytidylic acid; Pam 3 CSK 4 tripalmitoyl-S-glycero-Cys-(Lys)4; RF risk factor; R848 Imidazoquinoline Resiquimod; SEB staphylococcal enterotoxin B; TC T cell; TCR T cell receptor; Th17 T helper 17 cell; TLR Toll-like receptors; SPA staphylococcal protein A; TNF tumor necrosis factor; TGF-β transforming growth factor beta