Frontiers in immunology · 2026
Differential generation of parasite-specific Th2 and T follicular helper cells distinguishes resistant and susceptible mouse strains.
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Zhang Hongwei, Adjah Joshua, Kapse Bhavya, Affinass Nicole, Ebner Friederike, Hartmann Susanne, Rausch Sebastian
Аннотация
BACKGROUND: Both T helper 2 (Th2) and B cell responses are crucial for controlling gastrointestinal (GI) nematode infections. However, adaptive immune determinants of host susceptibility to GI nematode infection are still not fully understood.
METHODS: Adaptive immune responses against the small intestinal nematode Heligmosomoides polygyrus bakeri were compared between susceptible C57BL/6 and resistant BALB/c mice. Parasite-specific Th2 responses were quantified via combined detection of CD40-L and type 2 cytokine expression in CD4+GATA-3high cells stimulated with parasite products. Follicular T helper cell (TFH) and germinal center B cell responses were determined in parallel. Potential effects of the different Treg activity evident early during infection were tested by IL-2-induced Treg expansion in C57BL/6 and transient Treg depletion in BALB/c DEREG mice, respectively.
RESULTS: Both mouse lines generated comparable Th2 responses, but GATA-3+ Th2 cells comprised significantly higher proportions of parasite-specific cells in the more resistant BALB/c line. In addition, BALB/c mice exhibited stronger TFH responses and more rapid differentiation of IgG1+ germinal center B cells. The superior quality of the adaptive responses was accompanied by the early expansion of Foxp3+ Treg in BALB/c mice. While B cell transfers conveyed partial resistance to primary infection in the BALB/c line, transient Treg depletion at the onset of infection neither altered the quality of the Th2 effector response nor the extent of TFH and IgG1+ B cell responses, nor the control of parasite fitness. In contrast, Th2 responses were repressed following IL-2-induced Treg expansion in C57BL/6 mice, including the further marginalization of parasite-specific responses.
CONCLUSION: Together, these results indicate that resistance to GI nematodes depends on the quality rather than the quantity of T helper cell responses.
METHODS: Adaptive immune responses against the small intestinal nematode Heligmosomoides polygyrus bakeri were compared between susceptible C57BL/6 and resistant BALB/c mice. Parasite-specific Th2 responses were quantified via combined detection of CD40-L and type 2 cytokine expression in CD4+GATA-3high cells stimulated with parasite products. Follicular T helper cell (TFH) and germinal center B cell responses were determined in parallel. Potential effects of the different Treg activity evident early during infection were tested by IL-2-induced Treg expansion in C57BL/6 and transient Treg depletion in BALB/c DEREG mice, respectively.
RESULTS: Both mouse lines generated comparable Th2 responses, but GATA-3+ Th2 cells comprised significantly higher proportions of parasite-specific cells in the more resistant BALB/c line. In addition, BALB/c mice exhibited stronger TFH responses and more rapid differentiation of IgG1+ germinal center B cells. The superior quality of the adaptive responses was accompanied by the early expansion of Foxp3+ Treg in BALB/c mice. While B cell transfers conveyed partial resistance to primary infection in the BALB/c line, transient Treg depletion at the onset of infection neither altered the quality of the Th2 effector response nor the extent of TFH and IgG1+ B cell responses, nor the control of parasite fitness. In contrast, Th2 responses were repressed following IL-2-induced Treg expansion in C57BL/6 mice, including the further marginalization of parasite-specific responses.
CONCLUSION: Together, these results indicate that resistance to GI nematodes depends on the quality rather than the quantity of T helper cell responses.