Figure 3.
Impact of proximal TCR signaling defects on thymic development. (A) Left: Spatial organization of thymic microenvironments from cortex to medulla, with zones of positive and negative selection indicated. Right: Comparison of normal versus null/hypomorphic LCK thymi (in cross section). LCK deficiency impairs αβ lineage output (CD4 SP, CD8 SP, and Treg), while γδ T and NKT cells are reduced but preserved; MAIT cell status remains uncertain. (B) Mouse models of proximal TCR signaling defects, showing stage of developmental block and resulting thymic architecture. CMJ, corticomedullary junction. Refer to the image caption for details. Panel A: A diagram comparing the spatial organization of thymic microenvironments in normal and hypomorphic LCK thymus structures. On the left, the normal LCK thymus shows zones of positive and negative selection with various cell types, including DN, DP, CD8 SP, CD4 SP, Treg, MAIT, gamma delta T, and NKT cells. On the right, the hypomorphic LCK thymus shows impaired lineage output with reduced or absent CD8 SP, CD4 SP, Treg cells, and uncertain MAIT cell status, while gamma delta T and NKT cells are reduced but preserved. Panel B: A table listing mutations, their developmental arrest stages, and resulting thymic architecture. The table includes columns for mutation types, developmental arrest stages, and thymic architecture descriptions.

Impact of proximal TCR signaling defects on thymic development. (A) Left: Spatial organization of thymic microenvironments from cortex to medulla, with zones of positive and negative selection indicated. Right: Comparison of normal versus null/hypomorphic LCK thymi (in cross section). LCK deficiency impairs αβ lineage output (CD4 SP, CD8 SP, and Treg), while γδ T and NKT cells are reduced but preserved; MAIT cell status remains uncertain. (B) Mouse models of proximal TCR signaling defects, showing stage of developmental block and resulting thymic architecture. CMJ, corticomedullary junction.

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