Memory T cells, which are generated after the primary immune response to cognate antigens, possess unique features compared to naïve or effector T cells. These memory T cells are maintained for a long period of time and robustly reactivate in lymphoid or peripheral tissues where they re-encounter antigens. Environments surrounding memory T cells are importantly involved in the process of the maintenance and reactivation of these T cells. Although memory T cells are generally believed to be formed in response to acute infections, the pathogenesis and persistence of chronic inflammatory diseases, including allergic diseases, are also related to the effector functions of memory CD4 T cells. Thus, the factors involved in the homeostasis of allergen-specific memory CD4 T cells need to be understood to surmount these diseases. Here, we review the characteristics of allergen-specific memory CD4 T cells in allergic diseases and the importance of extrinsic factors for the homeostasis and reactivation of these T cells in the view of mediating persistence, recurrence, and aggravation of allergic diseases. Overall, this review provides a better understanding of memory CD4 T cells to devise effective therapeutic strategies for refractory chronic inflammatory diseases.

No abstract

Memory T (T M ) cells play an important role in the long-term defense against pathogen reinvasion. However, it is still unclear how these cells receive the crucial signals necessary for their longevity and homeostatic turnover. To understand how T M cells receive these signals, we infected mice with lymphocytic choriomeningitis virus (LCMV) and examined the expression sites of neural cadherin (N-cadherin) by immunofluorescence microscopy. We found that N-cadherin was expressed in the surroundings of the white pulps of the spleen and medulla of lymph nodes (LNs). Moreover, T M cells expressing high levels of killer cell lectin-like receptor G1 (KLRG1), a ligand of N-cadherin, were co-localized with N-cadherin + cells in the spleen but not in LNs. We then blocked N-cadherin in vivo to investigate whether it regulates the formation or function of T M cells. The numbers of CD127 hi CD62L hi T M cells in the spleen of memory P14 chimeric mice declined when N-cadherin was blocked during the contraction phase, without functional impairment of these cells. In addition, when CD127 lo KLRG1 hi T M cells were adoptively transferred into anti-N-cadherin-treated mice compared with control mice, the number of these cells was reduced in the bone marrow and LNs, with out functional loss. Taken together, our results suggest that N-cadherin participates in the development of CD127 hi CD62L hi T M cells and homing of CD127 lo KLRG1 hi T M cells to lymphoid organs.