CCR6-deficient mice have impaired leukocyte homeostasis and altered contact hypersensitivity and delayed-type hypersensitivity responses

CCR6-deficient mice have impaired leukocyte homeostasis and altered contact hypersensitivity and delayed-type hypersensitivity responses.

CCR6 expression in dendritic, T, and B cells suggests that this beta-chemokine receptor may regulate the migration and recruitment of antigen-presenting and immunocompetent cells during inflammatory and immunological responses. Here we demonstrate that CCR6-/- mice have underdeveloped Peyer's patches, in which the myeloid CD11b+ CD11c+ dendritic-cell subset is not present in the subepithelial d...

Inhibition of delayed-type contact hypersensitivity in mice deficient in both E-selectin and P-selectin.

Leukocyte rolling and emigration in response to inflammatory stimuli appears to involve both E-selectin- and P-selectin-dependent adhesion, which suggests that these molecules have overlapping functions. To clarify their relative contributions in chronic inflammation, we examined delayed-type contact hypersensitivity (DTH) responses in P-selectin, E-selectin, and E-/P-selectin-deficient mice. O...

Clinical aspects of contact hypersensitivity

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Hypersensitivity Responses in Compromised Humoral and Delayed-Type

Oral tolerance for delayed type hypersensitivity contribution of local and peripheral mechanisms

Oral tolerance is a physiological immune mechanism, which controls the outcome of deleterious hypersensitivity reactions to environmental antigens absorbed through the gastrointestinal tract, and maintains homeostasis. Using a mouse model of oral tolerance of delayed type hypersensitivity to contact allergens, i.e. haptens, we have examined the mechanisms involved in the induction of oral toler...