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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.
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
B-cell subsets can also express homing receptors that may allow their selective homing to particular types of tissue. A recent discovery concerns B cells that produce the immunoglobulin isotype IgA. IgA is an immunoglobulin type that is specialized to be present in fluids that are secreted by the body (e.g. tears, breast milk, intestinal mucus, lung mucus). The small subset of differentiated B cells that secrete IgA express the chemokine receptor CCR10, which is only rarely expressed by B cells that secrete other immunoglobulin isotypes.46,47 A ligand for CCR10, CCL28, is preferentially expressed by mucosal tissues from which IgA is secreted.44,48,49 Thus, CCR10 may be a homing receptor that allows IgA-secreting B cells to home to the tissues where IgA would be the most useful.
Serum CCL28 as a biomarker for diagnosis and evaluation of Sjögren’s syndrome
Published in Scandinavian Journal of Rheumatology, 2023
X Yu, F Zhu, X Yu, J Wang, B Wu, C Li
CCL28 is a chemokine that is widely expressed in human salivary glands, breast, colon, and bronchus, and its receptor is CCR10 (13). CCL28 recruits circulating IgA+ antibody-secreting cells expressing CCR10 by binding with the receptor, and participates in mucosal immunity by secreting secretory IgA antibodies in saliva and milk (14). In addition, CCL28 can directly exert its anti-bacterial and bacteriostasis roles and participate in mucosal immunity to effectively kill C. albicans, P. aeruginosa, S. mutans, etc. SS is a disease in which lacrimal and salivary glands are destroyed by lymphocytes. The ruined glands may lead to a decrease in CCL28 expression. Hernandez-Molina et al demonstrated that the expression of CCL28 in saliva of patients is lower than that in healthy people (4). However, since many patients with SS have no saliva as a result of gland damage (15), it is necessary to determine the expression of CCL28 in the serum of SS patients.
Comparing respiratory syncytial virus and rhinovirus in development of post-viral airway disease
Published in Journal of Asthma, 2022
Deepika Narayanan, Mitchell H. Grayson
The potential mechanism of RSV and the immune pathway involved has been studied by using Sendai virus (SeV) in murine models; SeV is genetically related to RSV so the mechanism of disease with SeV could be representative of that seen with RSV. When mice are infected with Sendai virus (SeV), airway epithelial cells release type I interferons (IFNα/β), which, although having an antiviral effect, can often lead to epithelial cell death, with the dead epithelial cells being eventually engulfed by macrophages (13). The chemokine, CCL5 (RANTES) protects macrophages from virus-induced death, effectively allowing them to participate in phagocytic viral clearance (14). In propagating acute post-viral disease, CD49d + neutrophils are recruited to the airway, where they are able to induce expression of the high affinity IgE receptor, FcεRI, on lung conventional dendritic cells (DC) (13,15). Next, anti-SeV IgE is produced, which binds to the DC expressed FcεRI, and then can be crosslinked by SeV, leading to release of the chemokine CCL28 (13). CCL28 attracts Th2 cells that then produce IL-13 (16). IL-13 is involved in the propagation of chronic post-viral airway disease (13,17). However, Th2 IL-13 production is not required in the SeV model as IL-13 can be produced by iNKT (invariant natural killer T cells) and then by a subset of activated macrophages (13,17). Macrophage activation requires iNKT production of IL-13, and when macrophages are activated by IL-13 (through IL-13Rα), they produce more IL-13 (17). IL-13 acts on the airway to drive mucous cell metaplasia and airway hyperreactivity (17).
Vasculogenic mimicry structures in melanoma support the recruitment of monocytes
Published in OncoImmunology, 2022
Lih Y. Tan, Michaelia P. Cockshell, Eli Moore, Kay K. Myo Min, Michael Ortiz, M. Zahied Johan, Brenton Ebert, Andrew Ruszkiewicz, Michael P. Brown, Lisa M. Ebert, Claudine S. Bonder
Interestingly, despite expressing the adhesion molecules required to mediate T cell recruitment (including ICAM-1 and JAM), we did not observe enhanced T-cell recruitment by VM competent melanoma cells under flow conditions. This can potentially be explained by their chemokine profile. In particular, melanoma cells did not express detectable levels of CXCL9, CXCL10 and CXCL11, which are known to interact with their receptor CXCR3 on T cells. This finding is important because CXCR3 has been reported to play a non-redundant role in controlling CD8+ T cell trafficking to human and murine melanoma and the absence of this signaling axis leads to impaired T cell recruitment and cancer progression.16 In contrast, all three melanoma cell lines expressed the chemokines CX3CL1 and CXCL16 at the gene and protein level, and expression of these chemokine genes was abundant within patient melanoma tissues. Both CX3CL1 and CXCL16 have been implicated in the recruitment of myeloid cells into tumors,58,59 and their receptors (CX3CR1 and CXCR6, respectively) are expressed by blood monocytes.60,61 Interestingly, CCL28 exhibited the highest correlation coefficient with MITF in TCGA human melanoma samples and was the only chemokine to exhibit increased expression in response to hypoxia in all of the melanoma cell lines tested (albeit marginally for the C32 and SK-Mel-28 cells). The role of CCL28 in melanoma is yet to be fully elucidated, but potential modes of action documented in other cancer types include cancer cell proliferation62 and tumor associated angiogenesis,63,64 investigating this further is a future direction of our work. One limitation of our study was to use supernatants from cancer cell cultures to profile the chemokine proteins. It is possible that some chemokine proteins are stored within intracellular granules or exosomes, investigating this further is another future direction of our work.