Abstract
In response to pathological challenge, the host generates rapid, protective adaptive immune responses while simultaneously maintaining tolerance to self and limiting immune pathology. Peripheral tissues (e.g., skin, gut, lung) are simultaneously the first site of pathogen-encounter and also the location of effector function, and mounting evidence indicates that tissues act as scaffolds to facilitate initiation, maintenance, and resolution of local responses. Just as both effector and memory T cells must adapt to their new interstitial environment upon infiltration, tissues are also remodeled in the context of acute inflammation and disease. In this review, we present the biochemical and biophysical mechanisms by which non-hematopoietic stromal cells and extracellular matrix molecules collaborate to regulate T cell behavior in peripheral tissue. Finally, we discuss how tissue remodeling in the context of tumor microenvironments impairs T cell accumulation and function contributing to immune escape and tumor progression.
Highlights
Immune surveillance and protective immunity is dependent upon sequential, rapid activation, and mobilization of hematopoietic cells that undergo multiple intercellular interactions to mediate immune control
De novo T cell priming is initiated in lymph nodes (LN) that drain peripheral sites of infection, inflammation, and tumors
Lymph-borne antigen is transported to LNs through afferent lymphatic vessels that connect to the subcapsular sinus allowing delivery of large particulate antigens (>70 kDa) to interfollicular dendritic cells (DC) and subcapsular macrophages [1, 2]
Summary
Peripheral tissues (e.g., skin, gut, lung) are simultaneously the first site of pathogen-encounter and the location of effector function, and mounting evidence indicates that tissues act as scaffolds to facilitate initiation, maintenance, and resolution of local responses. Just as both effector and memory T cells must adapt to their new interstitial environment upon infiltration, tissues are remodeled in the context of acute inflammation and disease. We discuss how tissue remodeling in the context of tumor microenvironments impairs T cell accumulation and function contributing to immune escape and tumor progression
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