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Phenomena as diverse as tuberculin sensitivity, delayed sensitivity to soluble proteins other than tuberculin, contact allergy, homograft rejection, experimental autoallergies, and the response to many microorganisms, have been classified as members of the class of immune reactions known as delayed or cellular hypersensitivity. Similarities in time course, histology, and absence of detectable circulating immunoglobulins characterize these cell-mediated immune reactions in vivo. The state of delayed or cellular hypersensitivity can be transferred from one animal to another by means of sensitized living lymphoid cells (CHASE, 1945; LANDSTEINER and CHASE, 1942; MITCHISON, 1954). The responsible cell has been described by GOWANS (1965) as a small lymphocyte. Passive transfer has also been achieved in the human with extracts of sensitized cells (LAWRENCE, 1959). The in vivo characteristic of delayed hypersensitivity from which the class derives its name is the delayed skin reaction. When an antigen is injected intradermally into a previously immunized animal, the typical delayed reaction begins to appear after 4 hours, reaches a peak at 24 hours, and fades after 48 hours. It is grossly characterized by induration, erythyma, and occasionally necrosis. The histology of the delayed reaction has been studied by numerous investigators (COHEN et al., 1967; GELL and HINDE, 1951; KOSUNEN, 1966; KOSUNEN et al., 1963; MCCLUSKEY et al., 1963; WAKSMAN, 1960; WAKSMAN, 1962). Initially dilatation of the capillaries with exudation of fluid and cells occurs.
The interplay between tumors and their immunologic microenvironment is complex, difficult to decipher, but its understanding is of seminal importance for the development of novel prognostic markers and therapeutic strategies. The present review discusses tumor-immune interactions in several human cancers that illustrate various aspects of this complexity and proposes an integrated scheme of the impact of local immune reactions on clinical outcome. Current active immunotherapy trials have shown durable tumor regressions in a fraction of patients. However, clinical efficacy of current vaccines is limited, possibly because tumors skew the immune system by means of myeloid-derived suppressor cells, inflammatory type 2 T cells and regulatory T cells (Tregs), all of which prevent the generation of effector cells. To improve the clinical efficacy of cancer vaccines in patients with metastatic disease, we need to design novel and improved strategies that can boost adaptive immunity to cancer, help overcome Tregs and allow the breakdown of the immunosuppressive tumor microenvironment.
Binding of various ligands (hormones, neurotransmitters, immunological stimuli) to membrane receptors induces the following changes: 1. Receptor redistribution (clustering, "capping") 2. Conformational changes that can be detected by fluorescent probes 3. Alteration in membrane fluidity (spin label and fluorescence polarization probes) 4. Changes in fluxes of ions and metabolites 5. Increased phospholipid turnover (especially of phosphatidyl inositol) 6. Activation of membrane-bound enzymes (adenyl cyclase, ATPase, transmethylases). Some of the early changes resulting from or associated with the binding (adsorption) of virions to the host cell membrane are of the same type. Adsorption of animal viruses to cells is the ftrst step in a chain of events resulting in the production of progeny virus on the one hand and in damage to cells and tissues on the other. In the classical studies of viral infection, cells are adsorbed with virus, usually for 60 min, and the changes induced by the virus in the host cell are recorded thereafter. In the past decade, more and more studies have been aimed at the events occurring in these ftrst 60 min of the so-called adsorption period. These studies deal with the nature of adsorption, e. g. , the ligand-receptor type of interaction between the virus and the cell membrane. Many receptors for viruses were identifted and so were the viral proteins which take part in adsorption.
Expression of an immune response is the net result of complex synergis tic and antagonistic activities performed by a variety of cell types. It includes macrophages, T and B populations which may interact in performance of a response, and suppressor cells interfering with it. Accordingly, a lack of res ponse may not necessarily indicate absence of immunocompetent cells, but rather nonexpression of competence. Thus, one should consider two possible situations, which are by no means mutually exclusive, to account for immuno logic unresponsiveness: (a) one or more of the cell populations composing the synergistic unit is absent or immature, and (b) an antagonistic unit which interferes with the response is dominating. In view of this, an approach to development of immune reactivity necessitates parallel surveys of development of cells with the potential to perform, as well as of cells which can suppress the response. Classification of the various cell types has been based so far on their phenotypic properties (e. g. , membrane antigen markers, cell receptors, pro duction and secretion of immunoglobulins, etc. ). Genotypically, T and B cells may represent either separate, independent cell lines, or different stages of development within the same cell lineage.