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Enrichment for a CD26 hi SIRP − subset in lymph dendritic cells from the upper aero‐digestive tract
Author(s) -
Epardaud Mathieu,
Bonneau Michel,
Payot Fabrice,
Cordier Corinne,
Mégret Jérôme,
Howard Chris,
SchwartzCornil Isabelle
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0404223
Subject(s) - lymph , biology , lymphatic system , dendritic cell , immune system , cholera toxin , lymph node , immunology , pathology , medicine , endocrinology
Dendritic cells (DC) have been reported to migrate in afferent lymph in the steady state. However, it is unknown whether DC traffic is modulated by the nature of the drained tissue. To analyze the influence of mucosal versus cutaneous microenvironments on the constitutive DC release, we exploited a novel technique of lymph cannulation in sheep, which allowed a comparison of afferent lymph DC migrating from the head mucosae [cervical DC (CerDC)] with DC migrating from skin [prescapular DC (PresDC)]. The migration rate was lower for CerDC than for PresDC. Compared with PresDC, CerDC contained a higher proportion of the CD26 hi signal regulatory protein (SIRP) − DC subset. It is interesting that cytoplasmic apoptotic DNA as well as cytokeratin‐positive inclusions were primarily detected among CD26 hi SIRP − DC, an observation similar to that made in rats, which leads to the suggestion that this subset was involved in self‐antigen presentation and tolerance induction. After the inoculation of cholera toxin (CT) onto the oro‐nasal mucosae, migration of CD26 hi SIRP − and CD26 lo SIRP + DC was accelerated in lymph, indicating that the effect of CT on DC mobilization is not subset‐specific. Our results show that a mucosal environment influences DC output and the relative DC subset representation in lymph. This modulation of DC traffic to lymph nodes by mucosal surfaces is likely to affect the bias of the mucosal immune responses.

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