Role of syndecan-1 in the interaction between dendritic cells and T cells

Abstract

Syndecan-1 (Sdc-1) is a heparan sulfate proteoglycan that can bind cytokines and chemokines via its heparan sulfate side chains, and has immunomodulatory properties in experimental models. Sdc-1 expression has been reported on dendritic cells (DC) and T cells. The potential role of Sdc-1 in DC-T cell interaction has not been investigated yet. We postulate that Sdc-1 is involved in DC-T cell interaction and may influence graft survival in an allogeneic transplant model. Sdc-1 expression on bone marrow-derived DC and T cells was analyzed by flow cytometry. Unstimulated and LPS stimulated Sdc-1 deficient DC were evaluated in vitro for phenotype and stimulatory capacity in mixed lymphocyte reaction. Sdc-1 deficient T cells were evaluated for proliferative capacity and differentiation in a mixed lymphocyte reaction and a proliferation assay. Allograft survival was evaluated in a fully MHC mismatched heterotopic heart transplant model, with either Sdc-1 deficient donors or recipients. Sdc-1 was expressed on the cell surface of unstimulated and LPS matured DC. Sdc-1 deficiency had no effect on expression of co-stimulatory molecules, cytokine production or T cell stimulatory capacity as compared to WT DC. Sdc-1 expression was not detectable on WT T cells, although intracellular Sdc-1 expression could be demonstrated after ConA activation. Sdc-1 deficient T cells showed reduced proliferation upon DC or ConA stimulation and reduced IL-17 production upon ConA stimulation, compared to WT T cells. Sdc-1 deficiency of either allograft or recipient did not prolong allograft survival. In conclusion, Sdc-1 is expressed on the cell surface of DC, where its absence does not affect DC phenotype or T cell stimulatory capacity. Sdc-1 is intracellularly expressed in ConA activated T cells. Sdc-1 deficiency in T cells results in a reduced proliferative response in vitro, as induced by DC and ConA. Sdc-1 deficiency in donor or recipient does not affect allograft survival.

Single‐cell RNA‐seq reveals clonal diversity and prognostic genes of relapsed multiple myeloma

“…As expected, most of the CD138 + cells isolated by MACS were myeloma cells mixed with a few normal immunocytes, including T cells and monocytes (Figures S2‐6). Notably, the SDC1/CD138 gene product was identified as a weakly expressed in T cells in our study, which was consistent with previous findings that its expression was described in dendritic cells, activated T cells and macrophages 26–29 …”

“…Notably, the SDC1/CD138 gene product was identified as a weakly expressed in T cells in our study, which was consistent with previous findings that its expression was described in dendritic cells, activated T cells and macrophages. [26][27][28][29] As MM is a plasma cell neoplasm, myeloma cells undergo the same V(D)J recombination process and somatic hypermutation as B cells and often exhibit singlecell clonal amplification. 30 Next, we checked the malignant cell clonotypes through single-cell V(D)J sequencing data.…”

Syndecan receptors: pericellular regulators in development and inflammatory disease

“…Glypican 5 appears in DCs at all stages, but not monocytes or macrophages, while glypican-1 was absent only from monocytes [182]. A number of other studies confirmed the presence of all four syndecans on DCs by flow cytometry [183][184][185]. This expression data raises the possibility that at least in the context of monocytes, macrophages and DCs there are likely to be multiple GAGbearing molecules on the cell surface, conceivably bearing GAG chains with distinct, core protein-specified properties.…”

“…Leucocyte representations were generated with the aid of www.biorender.com. For references see [177][178][179][180][181][182][183][184][185][186][187][188][189][190][191][192][193].…”

Investigating the effects of Laggera pterodonta on H3N2-Induced inflammatory and immune responses through network pharmacology, molecular docking, and experimental validation in a mice model

“…SDC-1 has immunomodulatory capabilities and is essential in controlling lung inflammation [ 37 , 38 ]. The respiratory mucosa, including plasma cells, tissue-resident memory B cells, and plasmablasts, secretes the antibody IgA [ 39 ].…”