Endogenous CD83 Expression in CD4⁺ Conventional T Cells Controls Inflammatory Immune Responses

Area of Science:

• Immunology
• Cell Biology

Background:

• The glycoprotein CD83 is expressed on various immune cells, including regulatory T cells (Tregs) and conventional T cells.
• The precise physiological role of endogenous CD83 within CD4+ T cell subsets remains largely undetermined.

Purpose of the Study:

• To investigate the function of endogenous CD83 in CD4+ T cell subsets.
• To elucidate the impact of CD83 deficiency on T cell responses and associated inflammatory conditions.

Main Methods:

• Generation of a CD83flox mouse line for conditional CD83 ablation in T cells using CD4-cre mice.
• In vitro stimulation assays to assess T cell proliferation, cytokine secretion, and differentiation.
• In vivo models including contact hypersensitivity and adoptive transfer-induced colitis.

Main Results:

• CD83 deficiency did not impair Treg suppressive activity but enhanced conventional CD4+ T cell proliferation and IFN-γ secretion.
• T cell-specific CD83 ablation aggravated contact hypersensitivity and colitis, correlating with increased T cell activation and IL-12 production.
• CD83-deficient T cells promoted enhanced CD40 expression and IL-12 secretion by dendritic cells.

Conclusions:

• Endogenous CD83 in conventional CD4+ T cells is critical for controlling T cell responses.
• CD83 regulates T cell activation, differentiation, and inflammatory potential, partly through modulating dendritic cell function.
• These findings highlight CD83 as a key regulator in adaptive immunity and inflammatory processes.