Stephen D. Miller

Control of experimental contact sensitivity.

Publisher Summary This chapter discusses controls operative in the expression of experimental contact sensitivity. The events leading to contact sensitivity, including the essential reactivity of the antigen with self molecules, the involvement of Langerhans cells of the skin, and the eventual development of effector T lymphocytes are presented. The chapter focuses on several mechanisms influencing the extent of a sensitivity response. Controlling factors include (1) route and amount of antigen presentation, which to a great degree determine whether sensitization or tolerance will develop, (2) production of soluble suppressor substances that may accompany tolerogenic regimes of antigen administration, (3) formation of inhibitory antiidiotypic antibodies, and (4) development of T suppressor cells. These multiple regulatory mechanisms operating in contact sensitivity are quite similar to those involved in other cellular immune responses as well as in humoral responses and are in keeping with the general elaborate regulation controlling immunity. The chapter describes the regulatory and suppressive mechanisms that control the induction, magnitude, expression, or duration of the contact allergic reaction. Experimental contact sensitivity is a highly regulated immune response. Sensitization depends upon application of reactive antigens that couple covalently to self tissues.

Binding of ovalbumin to mouse spleen cells with and without carbodiimide

We studied the binding of ovalbumin (OVA) to mouse spleen cells. In the presence or absence of carbodiimide (ECDI), uptake increased with greater cell numbers, increasing OVA concentration and increasing time up to 60 min. Between 60 and 210 microgram OVA could be coupled with ECDI to 2 X 10(8) cells. In the absence of ECDI, however, OVA uptake was still appreciable, but appeared to be of low avidity as it did not occur in the presence of competing fetal calf serum. These experiments provide a basis for the use of protein coupled to autologous cells in the induction of immunologic tolerance.