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In their own defense, tissues send a panoply of signals that initiate immunity and guide the choice of effector class. TH1-TH2 and Treg is far too simple a representation of the breathtaking variety of the resulting responses.
Histone modification is an important means of 'fine tuning' gene expression. The Shigella flexneri dually specific phosphatase OspF shapes host inflammatory transcriptional responses by inducing epigenetic modifications.
Fungal infection is 'sensed' by host cell–expressed receptors. Two papers demonstrate that the C-type lectin receptor dectin-1 is required in vivo for cytokine production and killing of different fungal pathogens.
Loss of the aminopeptidase ERAAP produces a distinct repertoire of peptide–major histocompatibility complex class I complexes. That difference elicits frequencies of immune recognition in congenic mice similar to those in allogeneic immune responses.
The immune system has co-evolved with microbes that cause acute infectious disease. Immune responses must be appropriate to allow survival of both the individual and the species. These responses involve complex interactions that often go unmeasured.
Relapses and exacerbation of clinical symptoms are hallmarks of debilitating autoimmune diseases like multiple sclerosis. Osteopontin-induced survival of autoreactive T cells may be one mechanism underlying the clinical progression of autoimmune disease.
Communicating about and comprehending immune responses and immunity will be facilitated by greater attention to semantic precision and consistency and increased willingness to engage with the full dimensionality and quantitative nature of immunological phenomena.
