T cells are implicated in both local and systemic pathophysiology of primary Sjögren’s syndrome (PSS). Lymphocytic
infiltrates in exocrine glands are dominated by CD4+ T cells, some contributing to ectopic lymphoid tissue, others,
unusually, exhibiting cytotoxic potential. Cytokine secretion patterns are complex, with Th1 and Th17 components
implicated in pathology. Circulating T cells exhibit phenotypes consistent with hyperactivation, cytokine imbalance, and
homeostatic alterations; CD4 lymphopenia is recognized as a risk factor for developing lymphoma. Evidence of oligoclonal
expansion is found locally and systemically. Functional alterations (e.g. cytokine secretion profile, migratory potential,
target cell interactions) are less clearly defined. Attempts at T cell-targeted therapy of PSS have been limited, although
therapy targeted at other arms of the immune response may also affect T cells. A better understanding of T-cell
dysregulation in PSS is required in order to understand its contribution to disease, aid prognosis, and improve therapeutic
interventions aimed at this aspect of the disease.
Keywords: Autoimmune disease, cytokines, cytotoxicity, homeostasis, pathophysiology, Sjogren’s syndrome, T-cell activation,
T lymphocyte subset, systemic pathophysiology, ectopic lymphoid tissue, lymphoma, cytokine, aid prognosis, lymphocytes collaborate, tissue damage occurs.
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