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Gastrointestinal nematode (GIN) infection has applied significant evolutionary pressure to the mammalian immune system and remains a global economic and human health burden. Upon infection, type 2 immune sentinels activate a common antihelminth response that mobilizes and remodels the intestinal tissue for effector function; however, there is growing appreciation of the impact GIN infection also has on the distal tissue immune state. Indeed, this effect is observed even in tissues through which GINs never transit. This review highlights how GIN infection modulates systemic immunity through (a) induction of host resistance and tolerance responses, (b) secretion of immunomodulatory products, and (c) interaction with the intestinal microbiome. It also discusses the direct consequences that changes to distal tissue immunity can have for concurrent and subsequent infection, chronic noncommunicable diseases, and vaccination efficacy. [ABSTRACT FROM AUTHOR]

The article explores how Follicular helper T (TFH) cells are essential for generating protective humoral immunity. Topics discussed include thymocyte selection–associated HMG-box protein (TOX) was identified as a central transcription regulator in TFH cell development; TOX promotes the expression of multiple molecules that play critical roles in TFH cell differentiation and function; and understanding of the molecular mechanisms that govern the differentiation and function of TFH cells.