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Overview of the mucosal immune system structure
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Reinhard Pabst, Per Brandtzaeg
In addition to directing activated mucosal B cells to the intestinal lamina propria, CCR10 appears to be a unifying chemokine receptor contributing to homing of plasmablasts to extraintestinal secretory effector sites. Several recent studies have shown CCR10 is expressed by IgA+ plasmablasts (and less so by IgA+ plasma cells) at every mucosal effector site in humans and mice. This expression pattern also characterizes IgD+ plasmablasts/plasma cells in the upper airways, as well as IgM+ and IgG+ plasmablasts/plasma cells replacing the IgA+ plasma cells in the gut of IgA-deficient subjects. As previously mentioned, CCL28/MEC, the CCR10 ligand, is constitutively produced by gut epithelium, especially in the large bowel, and is also expressed at relatively high levels by secretory epithelia in the upper aerodigestive tract and lactating mammary glands. Interestingly, CCL28 (but not CCL25) was shown to attract tonsillar IgA+ plasmablasts in vitro. Therefore, graded tissue site-dependent CCR10–CCL28 interactions, together with insufficient levels of classical gut-homing molecules, most likely explain the observed dispersion dichotomy for memory/effector B cells derived from Waldeyer's ring. Because bone marrow stromal cells reportedly produce CCL28, interactions of this chemokine with CCR10+ B cells may furthermore contribute to integration between mucosal and systemic immunity.
Chemokines and Chemokine Receptor Interactions and Functions
Published in Thomas R. O’Brien, Chemokine Receptors and AIDS, 2019
Philip L. Shields, David H. Adams
Chemokines act via specific cell surface, seven transmembrane spanning G-protein-linked receptors (Figure 2). Five CXC chemokine receptors (CXCR1 to CXCR5), ten CC chemokine receptors (CCR1 to CCR10), and one CXXXC receptor have been identified so far in humans (Table 1). Most chemokine receptors are shared by more than one chemokine, such as CXCR3 which binds IP-10, MIG or IFN-inducible T cell alpha chemoattractant (I-TAC). A few have a restricted number of ligands such as CCR6 which binds MEP-3α and CXCR1, which binds IL-8 and granulocyte chemoattractant protein-2 (GCP-2). Some chemokines can also interact with more than one receptor (e.g., MIP-1α) suggesting a degree of redundancy and flexibility in the chemokine/chemokine receptor system. Engagement of chemokine receptors is associated with a calcium flux and G-protein dependent activation of phospholipases. The details of the downstream signals differ between cell types, so, for instance, IL-8 causes phospholipase D activation in lymphocytes, but not in neutrophils. There is also evidence that the consequences of receptor engagement is determined by the intracellular signals., Thus cytoskeletal rearrangement is a consequence of phospholipase C and Rho activation, whereas activation of protein tyrosine kinases is involved in cell activation and proliferation (11).
Lymphocyte homing and immunology of extranodal lymphoid tissues
Published in Franco Cavalli, Harald Stein, Emanuele Zucca, Extranodal Lymphomas, 2008
Mariagrazia Uguccioni, James J Campbell, Katrin Kuscher, Marshall E Kadin
While all naive cells share the same repertoire of adhesion molecules and chemoattractant receptors expressed on their surfaces, various subsets of memory cells express different repertoires of such homing molecules. The homing properties of memory cells are dependent upon the repertoire of homing molecules that they express.2,8 For example, approximately 20% of memory Th2 lymphocytes from human peripheral blood express the cutaneous lymphocyte antigen (CLA). CLA is a carbohydrate that allows lymphocytes to roll on E-selectin-expressing blood vessels. A separate ~20% of memory Th2 lymphocytes from blood express the α4β7-integrin (Figure 5.1).2,8 As discussed in the previous section, α4β7 allows rolling and adhesion within vessels expressing the mucosal addressin MAdCAM-1.14–16 There are essentially no Th2 cells that express both CLA and α4β7 together, so these markers define distinct populations. Similar contrasts are found for expression of chemokine receptors: CCR4 is found primarily on α4β7-negative Th2 cells,34–36 whereas CCR9 is found only on a subset of α4β7-positive Th2 cells.37 To complete the picture, cutaneous and intestinal tissues have differential expression of the ligands for these chemokine receptors and homing molecules.34,38 Study of lymphocytes isolated from surgical samples of such tissues confirm that co-expression of CLA and CCR4 defines the population of memory Th2 lymphocytes that is specialized to home through cutaneous sites.34–36 CCR10 is also expressed on a subset of cutaneous lymphocytes, and may also play a role in cutaneous homing.39 Co-expression of α4β7 and CCR9 defines a population of memory Th2 cells dedicated to homing to the small intestine.37,38,40
Expression of Homing Receptors in IgM+IgD+CD27+ B Cells and Their Frequencies in Appendectomized and/or Tonsillectomized Individuals
Published in Immunological Investigations, 2023
Diana Bautista, Consuelo Romero-Sánchez, Manuel Franco, Juana Angel
In humans, blood circulating IgM+IgD+CD27+ B cells are considered analogous to those described in the MZ of the spleen (Berkowska et al. 2011; Weill and Reynaud 2020). One way to explore whether these cells have the potential to home to GALT and NALT is by evaluating their expression of homing receptors (Habtezion et al. 2016). Several of these homing receptors have been described: α4β7 is a heterodimeric integrin expressed by T and B cells that mediates homing to the small intestine and colon (Habtezion et al. 2016). CCR9 binds to CCL25 expressed in the small intestine but absent in the colon (Briskin et al. 1997; Habtezion et al. 2016), and CD22 has been described as a homing receptor binding to a 2–6-sialylated glycan expressed in GALT and tonsils (Kimura et al. 2007). Finally, CCR10 is a chemokine receptor expressed on plasma cells homing to the jejunum, ileum, stomach, colon and appendix (Kunkel et al. 2003). Although, tonsil specific homing receptors are unidentified, plasma cells expressing CCR9 and CCR10 have been identified in this organ (Kunkel et al. 2003). A previous report showed co-expression of β7 (used as surrogate of α4β7 expression) and CCR9 on approximately 12% of circulating MZBC (Magri et al. 2017), but the expressions of CD22 and CCR10 are unreported.
Correlation analysis between IL-35, IL-36γ, CCL27 and psoriasis vulgaris
Published in Journal of Dermatological Treatment, 2021
Jiao Chen, Jiaxi Du, Yiyang Han, Zhiping Wei
Psoriasis is an immune inflammatory skin disease, which is maintained by a variety of pro-inflammatory pathways, where cytokines and chemokines produced by T cells and epidermal keratinocytes play a major role (18). CCL27 is a skin-specific CC-type chemokine expressed by keratinocytes. It is expressed only in the skin and not in other organs and is expressed constitutively especially in epidermal keratinocytes (19). It can be specifically expressed in skin homing associated antigen positive (CLA+) lymphocytes (20). CCL27 binds to chemokine receptor 10 (CCR10) on skin homing T cells and induces inflammation by promoting the migration of Th1 and Th2 lymphocytes to skin. It is believed that CCL27 plays a key role in T cell-mediated inflammation (21). In psoriatic lesions, suprabasal cells maintain strong CTACK/CCL27 expression due to accelerated proliferation and reduced differentiation (19). It has been reported that TNF-α can upregulate the expression of CTACK/CCL27 and promote the migration of skin lymphocyte-associated antigen positive lymphocytes to skin (19). However, IL-17 plays a key role in downregulating the expression of CCL27 in the late stage of plaque psoriasis. This experiment found that the expression of CCL27 in psoriasis patients was significantly higher than that in normal control group, and the expression was positively correlated with the severity of psoriasis. It is suggest that CCL27 may participate in the pathogenesis of psoriasis as a proinflammatory factor.
Innate lymphoid cells regulate radiation-induced skin damage via CCR10 signaling
Published in International Journal of Radiation Biology, 2020
Yiwen Mao, Rui Tao, Xiaoping Cao, Qin Bao, Dong Wang, Ye Zhao
CCR10 plays a very important role in skin immune response and inflammatory changes. Xia et al. demonstrated that compared to wild type mice, CCR10−/− mice had more severe skin inflammatory reactions in response to cutaneous stimulation by chemical irritants and infection by Leishmania due to dysregulation of skin regulatory and effector T cells (Xia et al. 2014). In this study, we tested the effect of CCR10 deletion on radiation-induced skin injury and radiation dermatitis in mice. The radiosensitivity of mice is less than human, and our preliminary experiments found that radiation of 2 Gy/fraction were difficult to induce acute radiodermatitis in mice. In this study, we use 5 Gy/fraction to induced acute inflammation of mouse skin. And 6 × 5 Gy were used to study chronic inflammation of mouse skin. CCR10+/− and CCR10−/− mice were irradiated by a single dose of 5 Gy of X-ray to induce the acute dermatitis, which does not kill a lot of immune cells. Although the ratios of ILCs decreased in both CCR10+/− and CCR10−/− mice 3 days after irradiation, there was no significant difference in the proportion of ILCs between CCR10+/− and CCR10−/− mice at the same time point. The skin inflammation disappeared and ILCs restored to normal levels 10 days after single irradiation. These results suggested that local inflammatory changes were alleviated and that the irradiated skin were gradually recovered with time. These results indicate that CCR10 might not play an important role in regulating ILCs under single irradiation.