Help Is on the Way: Recruitment of Helper T Cells to Peripheral Tissues

Helper T cells leaving secondary lymphoid tissues to provide effector functions in peripheral tissues undergo changes in chemokine receptor expression, allowing them to migrate to specific sites of inflammation or infection. The chemokine receptors involved in this process include CCR7 and CXCR4, which are typically expressed by naïve and central memory T cells, facilitating their retention within lymphoid tissues. However, effector and effector memory T cells downregulate CCR7 and CXCR4 and upregulate other chemokine receptors, such as CCR5, CXCR3, and CCR6, enabling their migration to peripheral tissues in response to inflammatory signals.

Different subsets of helper T cells may indeed express different combinations of chemokine receptors, reflecting their specialized functions and migratory patterns. For instance:

  1. Th1 cells: These cells express CXCR3, which directs their migration to sites of inflammation where the ligands for CXCR3, such as CXCL9, CXCL10, and CXCL11, are upregulated, such as in response to viral infections or autoimmune diseases.
  2. Th2 cells: Th2 cells may express CCR4, which guides them to sites where the ligands for CCR4, such as CCL17 and CCL22, are produced, such as in allergic reactions or parasitic infections.
  3. Th17 cells: Th17 cells often express CCR6, which plays a role in their recruitment to mucosal tissues, including the gut and lungs, where the ligand for CCR6, CCL20, is abundantly expressed.
  4. Treg cells: Regulatory T cells express distinct chemokine receptors, such as CCR4 and CCR8, which contribute to their recruitment to sites of inflammation or tolerance induction.

These are just a few examples, and the chemokine receptor expression profile of helper T cell subsets can vary depending on the specific microenvironment and the signals present during differentiation and activation.

Next Topic: Effector T Cell Functions in Peripheral Tissues

Source: ChatGPT response prompted and edited by Joel Graff.

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