ADOPTIVE CELL TRANSFER OF CONTACT SENSITIVITY-INITIATION MEDIATED BY NONIMMUNE CELLS SENSITIZED WITH MONOCLONAL IGE ANTIBODIES - DEPENDENCEON HOST SKIN MAST-CELLS
H. Matsuda et al., ADOPTIVE CELL TRANSFER OF CONTACT SENSITIVITY-INITIATION MEDIATED BY NONIMMUNE CELLS SENSITIZED WITH MONOCLONAL IGE ANTIBODIES - DEPENDENCEON HOST SKIN MAST-CELLS, The Journal of immunology, 154(10), 1995, pp. 5080-5092
A role for mast cell release of serotonin (5-HT), via Ag-specific fact
ors derived from Thy-1(+) B220(+) lymphoid cells in the initiation of
murine contact sensitivity (CS) has been suggested. However, because C
S in mast cell-deficient mice was intact, a role for mast cells in CS
initiation was unclear. Therefore, we examined whether CS could be ini
tiated by i.v. injection of nonimmune mixed lymphoid cells that were s
ensitized in vitro with IgE. When naive mice received IgE-sensitized n
onimmune spleen or lymph node cells, or IgE-sensitized purified mast c
ells, together with immune CS-effector B220(-) T cells, which therefor
e were depleted of CS-initiating, Thy-1(+), B220(+) cells, which could
not transfer CS, then reconstitution of CS occurred. Mast cell-deiici
ent W/W-v mice could not elicit this IgE-dependent CS ear swelling, bu
t when mast cell deficiency was reversed by ear injection of normal bo
ne marrow-derived cultured mast cells, then CS was restored. In vitro
pretreatment with irrelevant monoclonal anti-OVA IgE prevented CS init
iation mediated by Ag-specific, IgE mAb-sensitized cells, presumably b
y blocking sensitization with IgE. Thus Fc epsilon R on the normal lym
phoid cells were involved. When ketanserin, a 5-HT2 receptor antagonis
t, was injected i.v. before cell transfer, CS initiation via IgE-sensi
tized cells and CS were no longer elicited. Thus, in this system, IgE
Abs bound to circulating IgE Fc epsilon R bearing lymphoid cells sensi
tized in vitro (most likely basophils), probably mediated early activa
tion of these circulating basophils to release mediators, causing 5-HT
release from cutaneous mast cells, to mediate CS initiation.