HUT 78 T cells bind to noncytokine-stimulated keratinocytes using a non-CD18-dependent adhesion pathway

Area of Science:

• Immunology
• Dermatology
• Cell Biology

Background:

• T-cell interactions with skin cells are crucial in inflammatory skin diseases.
• Lymphocyte-function-associated antigen-1 (CD18) on T cells binds intercellular adhesion molecule-1 (CD54) on keratinocytes.
• Further investigation is needed into other adhesion mechanisms.

Purpose of the Study:

• To explore molecular interactions between T cells and skin cells (keratinocytes, fibroblasts, melanocytes).
• To investigate the role of cytokines and phorbol esters in modulating these interactions.
• To understand the complexity of T-cell trafficking in skin.

Main Methods:

• Used HUT 78 and Jurkat T-cell lines.
• Co-cultured T cells with human keratinocytes, fibroblasts, and melanocytes.
• Treated skin cells with cytokines (gamma interferon) and/or phorbol ester.
• Assessed T-cell binding under various temperature conditions and in the presence/absence of antibodies.

Main Results:

• HUT cells bound keratinocytes without cytokine pretreatment, independent of CD18 and temperature.
• Fibroblasts and melanocytes also bound HUT cells, with fibroblast binding being temperature-sensitive.
• Cytokine/phorbol ester treatment induced a "superadhesive" state in keratinocytes, increasing T-cell binding via enhanced CD54 expression.
• Qualitative and quantitative differences observed in T-cell binding to different skin cells and treatment conditions.

Conclusions:

• T-cell interactions with skin cells involve multiple adhesion molecules and pathways.
• Cytokine-induced changes in keratinocytes significantly enhance T-cell adhesion.
• These findings highlight the complex molecular basis of T-cell trafficking in dermal and epidermal compartments.