Abstract
Immunological memory is a hallmark of adaptive immunity. Memory CD4 T cells function as a control tower of the adaptive immune system to direct immune responses, leading to the elimination of various invaded microorganisms. Important roles of functionally distinct CD4 helper T cell (Th) subsets, such as Th1, Th2 and Th17 cells, in the host-defense immune responses have been well recognized. In addition, however, these Th cell subsets are known to be involved in the pathogenesis of various chronic inflammatory diseases, including asthma. We recently identified an IL-5-producing highly pathogenic population in memory Th2 cells in allergic asthma [1, 2]. We named this population “memory-type pathogenic Th2 (Tpath2) cells” in airway inflammation. Other investigators also reported distinct Th2 cell populations, which produce a substantial amount of IL-5 or multiple cytokines in addition to IL-4 and IL-13 [3, 4]. These populations appear to be responsible for the pathology of various Th2-type chronic inflammatory diseases.
Highlights
Immunological memory is a hallmark of adaptive immunity
We have recently shown that IL-33 confers the pathogenicity of memory Th2 cells by inducing p38 mitogen-activated protein kinase (MAPK) activation [5]
We need to wait a precise analysis, an interesting possibility is that memory Th2 cells have acquired newly induced molecules in signaling or machinery in chromatin remodeling processes in addition to the increased expression of ST2. p38 MAPK is identified as the downstream target of IL33-ST2 signaling
Summary
Immunological memory is a hallmark of adaptive immunity. Memory CD4 T cells function as a control tower of the adaptive immune system to direct immune responses, leading to the elimination of various invaded microorganisms. Recent studies on the functional clarification of memory Th2 cell subpopulations identified that distinct IL-5-producing memory-type Th2 cell subpopulations induced eosinophilic inflammation such as allergic airway inflammation and chronic skin inflammation [1, 3]. Memory-type Th2 subpopulations appear to contribute to the pathogenesis and persistence of chronic airway inflammation such as chronic asthma and chronic skin inflammation.
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