Abstract
Tissue resident memory T (TRM) cells reside in peripheral, non-lymphoid tissues such as the skin, where they act as alarm-sensor cells or cytotoxic cells. Physiologically, skin TRM cells persist for a long term and can be reactivated upon reinfection with the same antigen, thus serving as peripheral sentinels in the immune surveillance network. CD8+CD69+CD103+ TRM cells are the well-characterized subtype that develops in the epidermis. The local mediators such as interleukin (IL)-15 and transforming growth factor (TGF)-β are required for the formation of long-lived TRM cell population in skin. Skin TRM cells engage virus-infected cells, proliferate in situ in response to local antigens and do not migrate out of the epidermis. Secondary TRM cell populations are derived from pre-existing TRM cells and newly recruited TRM precursors from the circulation. In addition to microbial pathogens, topical application of chemical allergen to skin causes delayed-type hypersensitivity and amplifies the number of antigen-specific CD8+ TRM cells at challenged site. Skin TRM cells are also involved in the pathological conditions, including vitiligo, psoriasis, fixed drug eruption and cutaneous T-cell lymphoma (CTCL). The functions of these TRM cells seem to be different, depending on each pathology. Psoriasis plaques are seen in a recurrent manner especially at the originally affected sites. Upon stimulation of the skin of psoriasis patients, the CD8+CD103+CD49a- TRM cells in the epidermis seem to be reactivated and initiate IL-17A production. Meanwhile, autoreactive CD8+CD103+CD49a+ TRM cells secreting interferon-γ are present in lesional vitiligo skin. Fixed drug eruption is another disease where skin TRM cells evoke its characteristic clinical appearance upon administration of a causative drug. Intraepidermal CD8+ TRM cells with an effector-memory phenotype resident in the skin lesions of fixed drug eruption play a major contributing role in the development of localized tissue damage. CTCL develops primarily in the skin by a clonal expansion of a transformed TRM cells. CD8+ CTCL with the pagetoid epidermotropic histology is considered to originate from epidermal CD8+ TRM cells. This review will discuss the current understanding of skin TRM biology and their contribution to skin homeostasis and diseases.
Highlights
The number of T cells infiltrating in the skin is nearly twice as many as that in the peripheral blood, and the majority of these cells are effector memory T cells [1]
One of the important issues on the residency status of skin Resident memory T cell (TRM) cells in which what conditions allow TRM cells to emigrate from the tissue is under debate
Skin TRM fate decision seems to be established prior to antigens recognition. Once these naïve T cells encounter with cognate antigen presented by dendritic cells (DCs), these preconditioned T cells will be ready to become a skin-homing TRM precursor, implying that preconditioned naïve TRM cells are prepared during homeostasis, and skin-homing molecules are imprinted during T cell priming [89]
Summary
Yoshiki Tokura 1,2*, Pawit Phadungsaksawasdi 1, Kazuo Kurihara 1, Toshiharu Fujiyama 1 and Tetsuya Honda 1. Reviewed by: Wolfgang Kastenmüller, Julius Maximilian University of Würzburg, Germany Phillip Scott, University of Pennsylvania, United States. Specialty section: This article was submitted to Immunological Memory, a section of the journal
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