Immune serum from mice contact‐sensitized with picryl chloride contains an antigen‐specific T cell factor that transfers immediate cutaneous reactivity

Abstract

This report describes an activity in serum from mice that were contact-sensitized with picryl chloride (PCl) 1 to 4 days earlier. Immune serum, when given i.v., transfers the ability to elicit an immediate hypersensitivity-like ear swelling reaction in naive recipients following local challenge with PCl. This serum activity is due to an antigen-binding T cell factor that shares some properties with IgE antibody. The activity is antigen specific, and due to an antigen-binding moiety that is heat labile (56 degrees C, 4 h). However, unlike IgE antibody the serum activity is resistant to reduction and alkylation, and is retained by columns of Sepharose beads coupled with polyclonal or monoclonal antibodies that react with antigen-specific T cell factors from other systems. These columns did not retain IgE antibody activity in our experiments. Importantly, the serum activity was not retained by columns linked with antibodies directed to mouse immunoglobulins, which do retain IgE activity. We conclude from these data that the activity in PCl immune serum is not caused by IgE antibody, and is due to the presence of the previously described antigen-specific T cell factor (PCl-factor), that can activate serotonin-containing cells, such as mast cells, to release the vasoactive amine serotonin. PCl-factor transfers the ability to elicit an immediate hypersensitivity-like reaction that is an early component of delayed-type hypersensitivity. The presence of this T cell factor in the serum of actively sensitized mice provides a means to sensitize tissues throughout the body for this required, initial, serotonin-dependent component of delayed-type hypersensitivity reactions.

Serotonin Initiation of Delayed-Type Hypersensitivity: Mediation by a Primitive Thy-1⁺ Antigen-Specific Clone or by Specific Monoclonal IgE Antibody

“…and perhaps mast cells [7]. We employed induction of suppression of DTH with Ag-binding factors from the contact sensitivity system to examine whether the early allo-MHC-specific component of DTH was required for elicitation of DTH, and might thus be involved in immune resistance to an allograft tumor.…”

“…We have shown that DTH-initiating cells make Ag-specific DTH-initiating fac tors that we call, respectively: picryl chloride factor (PCI-F), and oxazolone factor (OX-F) [5,6,10,24]. These factors are not IgE anti bodies [6,7,9,10], nor are they dependent on IgE antibodies [10] UV tumor Ag-specific T cells were not able to transfer DTH, nor resistance to tumors. However, when combined with 1-day im mune DTH-initating cells of the Ag specific ity appropriate to a particular U V tumor, the specific DTH-initiating cells and the specific T cell line together were able to mediate immune resistance to the appropriate tumor [29].…”

“…After immunization they reside in the lymphoid tissues, and from these sites re lease an antigen-specific factor that has a biological activity analogous to IgE antibody [5,6]. This antigen-specific DTH-initiating factor can be found in the circulation [7] and subsequently in the extravascular tissues where it sensitizes serotonin (5HT)-containing cells [8][9][10], Thus, local Ag challenge causes release of 5HT [9. 10] to induce re cruitment and activation of CD4+ T cells that mediate DTH.…”

Differential Ability of Occupational Chemical Contact and Respiratory Allergens to Cause Immediate and Delayed Dermal Hypersensitivity Reactions in Mice

“…Apparent support for this proposal derives from evidence that reserpine, a drug that depletes mast cells of serotonin, markedly inhibits the elicitation of contact hypersensitivity [24,25], It has been further suggested that the early and late phases of dermal hypersensitivity reactions to contact allergens are, in the mouse, effected by the sequential action of two indepen dent antigen-specific populations of T lymphocytes [23,26]. The T lymphocyte responsible for inducing the early inflammatory response is considered to have a distinctive phenotype, and to produce an antigen-binding factor that sensitizes tissue mast cells in the manner of IgE [27][28][29][30][31], Following challenge, antigen is thought to bind to such sensitized mast cells, initiate degranulation and allow the infiltration of the second population of T lymphocytes that cause the late phase reaction [28,29], The concept of a mandatory requirement for early phase inflammation during the development of delayed hypersensitivity reactions remains controversial, however. It has been found, for instance, that mast cell-deficient mice exhibit delayed dermal hypersensitivity reactions comparable with those observed in normal animals [32][33][34].…”

Identification and Partial Characterization of a T-Cell-Derived Antigen-Binding Factor from Mice Infected with the Intestinal Helminth <i>Trichinella spiralis</i>

“…Polyclonality of TABM analogous to immunoglobulins is suggested by charge hetero geneity [8]; but the non-MHC-restricted TABM demonstrate similar characteristics [5,8,21]. TABM can be isolated from serum of sensitized mice [29] and are found on the surface of T cells, as well as in supernatants of lymphoid cell cultures [7,21,31] and display common serologic determinants [6,7], sug gesting a common isotype among antigen-specific T cell factors.…”