Donor effector T cell (Teff)

Donor effector T cells on the ocular surface are the primary cellular mediators of Ocular Graft-versus-Host Disease (oGVHD), a severe complication occurring after allogeneic hematopoietic stem cell transplantation (HSCT) (Ogawa et al., 2013). These donor-derived lymphocytes, particularly Th1 and Th17 subsets, migrate to and infiltrate the recipient's ocular tissues, including the lacrimal glands, conjunctiva, and cornea, in response to inflammatory signals and chemokines (Perez et al., 2013). Once present, they recognize host antigens and release pro-inflammatory cytokines such as interferon-gamma and interleukin-17, which drive chronic inflammation, goblet cell loss, and fibrosis of the lacrimal apparatus (Abidi et al., 2019). This process leads to severe dry eye disease, corneal scarring, and potential vision loss. Therapeutic interventions target these cells by inhibiting their activation (e.g., calcineurin inhibitors like cyclosporine), blocking their recruitment to the ocular surface (e.g., LFA-1 antagonists like lifitegrast), or modulating their signaling pathways (e.g., JAK inhibitors) (Shikari et al., 2013). Management of these cells is critical for preserving ocular surface integrity and patient quality of life post-transplant.

Other names

Donor T cellAlloreactive T cellEffector T lymphocyteOcular infiltrating lymphocyte

Inhibition of calcineurin-mediated T-cell activation; Antagonism of lymphocyte function-associated antigen-1 (LFA-1) to prevent T-cell adhesion and migration; Inhibition of Janus kinase (JAK) signaling to reduce cytokine production; Broad suppression of inflammatory gene expression via glucocorticoid receptor activation.