Gp. Geba et al., DELAYED-TYPE HYPERSENSITIVITY IN MAST CELL-DEFICIENT MICE - DEPENDENCE ON PLATELETS FOR EXPRESSION OF CONTACT SENSITIVITY, The Journal of immunology, 157(2), 1996, pp. 557-565
Previous studies of cutaneous T cell-mediated responses in mice have o
btained pharmacologic, morphologic, and immunologic evidence pointing
to a critical role for local mast cells in release of the vasoactive a
mine serotonin (5-HT) to mediate early, initiating events that are req
uired for elicitation of these responses. However, the role of mast ce
lls in initiating these T cell-mediated cutaneous responses has been q
uestioned due to the presence of relatively intact delayed-type hypers
ensitivity responses, such as contact sensitivity (CS), in mast cell-d
eficient mice whose skin contains only 1% normal mast cell numbers. Th
e contribution of other potential local sources of 5-HT, such as circu
lating platelets, at the site of a delayed-type hypersensitivity or CS
response in these mast cell-deficient strains, has not been investiga
ted. Therefore, we studied the effect of systemic platelet depletion,
produced with an anti-platelet Ab, on blood and tissue levels of 5-HT,
and on in vivo T cell-mediated cutaneous sensitivity responses, in W/
W-v and SI/SId mast cell-deficient mice. The results showed that: 1) p
latelet depletion severely reduced whole blood 5-HT; 2) tissue levels
of 5-HT, in mast cell-deficient mice, depended in large part on the pr
esence of circulating platelets, and 3) specific depletion of platelet
s markedly suppressed CS responses in both W/W-v and SI/SId mast cell-
deficient mice, and only moderately reduced CS in normal +/+ congenic
mast cell-sufficient controls, but did not decrease CS in beige mice,
with platelet granules that are defective in storage of 5-HT. We concl
uded that platelets may provide 5-HT crucial for the initiation of cut
aneous T cell-mediated immune responses, such as CS.