Renal tubular epithelial cells are constitutive non-cognate stimulators of resident T cells

Understanding the roles of different cell types in regulating T cell homeostasis in various tissues is critical for understanding adaptive immunity. Here, we show that RTECs (renal tubular epithelial cells) are intrinsically programmed to polyclonally stimulate proliferation of kidney ab T cells by a cell-cell contact mechanism that is major histocompatibility complex (MHC) independent and regulated by CD155, aVb3-integrin, and vitronectin. Peripheral CD4 and CD8 are resistant to RTEC-mediated stimulation, while the minor subset of double-negative (DN) T cells are responsive. This functional property of RTEC is discovered by using a coculture system that recapitulates spontaneous in vivo polyclonal proliferation of kidney T cells, which are mainly comprised of central memory T (TCM) and effector memory T (TEM) cells. This robust cell-intrinsic stimulatory role of RTECs could be underlying the steady-state spontaneous proliferation of kidney T cells. The results have conceptual implications for understanding roles of different cell types in regulating systemic and organ-specific T cell homeostasis.

Automated summary

Research on the regulation of kidney T cell proliferation by renal tubular epithelial cells (RTECs) reveals that RTECs stimulate polyclonal proliferation of kidney T cells through cell-cell contact, independent of major histocompatibility complex, and regulated by CD155, αVβ3 integrin, and vitronectin. Peripheral CD4 and CD8 show resistance to this stimulation, while the minor subset of double-negative (DN) T cells are responsive. This study has conceptual implications for understanding the role of different cell types in regulating systemic and organ-specific T cell homeostasis.