Publisher Summary This chapter describes membrane immunoglobulins and antigen receptors on B and T lymphocytes. There are several qualitative and quantitative distinctions between T-cell and B-cell M-Ig that may explain many of the apparent differences in reactivity of these cells without requiring the existence of a different set of V genes or non-Ig receptors in T cells. Both T and B cells derive from hematopoietic, precursor, stem cells by antigen-independent differentiation. This involves the activation of L-chain and p-type H-chain genes in both cell types. The T-cell and B-cell M-Ig differ primarily in density per cell and possibly in relative exposure on the cell surface with much of the H-chain Fc region inaccessible on T cells. Moreover, the antigen-recognition receptor of both T and B cells involves their M-Ig. On B cells, the receptor is solely the M-Ig, whereas on T cells it is suggested that the specificity of recognition controlled primarily by the M-Ig and binding of antigen to the cell can solely be by the M-Ig receptor. Finally, the activation of the T cell requires an additional interaction of the antigen with another ceIl surface structure that is coded for by a polymorphic H-2 linked gene.

Membrane immunoglobulins and antigen receptors on B and T lymphocytes.

The complement-mediated cytotoxicity assay has been used to demonstrate surface immunoglobulin determinants on human peripheral blood lymphocytes. In two individuals with monoclonal serum IgM components, idiotypic antisera demonstrated similar components on a significant proportion of the peripheral blood lymphocytes.

https://rupress.org/jem/article-pdf/136/3/650/1392897/650.pdf

Idiotypic determinants of immunoglobulin m detected on the surface of human lymphocytes by cytotoxicity assays

Selective destruction of alpha fetoprotein (AFP)-producing cells was based on the relative amount of AFP produced. In this case cytotoxic effect of horse antisera inactivated at 56 degrees C for 30 minutes on cultivated rat tumor cells (rat ascites hepatoma AH66) was evident by a selective inhibitory effect on growth of these AFP-producing cells. A portion however small of this cell population did survive and they gradually increased their number. These viable cells were found to be low AFP-producing. Repeated treatment with anti-AFP sera separated extremely low AFP-producing cells. When these very low producing cells were transplanted into rats survival time was 2 times as long as with the original AH66 cell line. Growth of high AFP-producing clones of AH66 was inhibited within 48 hours of cultivation. On the other hand growth of low AFP-producing clones was only slightly inhibited. Apparently anti-AFP antibody adhered to AFP secreted on the cell surface as shown by positive membrane immunofluorescence and this antigen-antibody complex binding on the cell surface may inhibit cell multiplication. A close correlation between cytotoxic index and rate of AFP production was found. No observable effect was found when complement was added to antisera under these experimental conditions.

Effect of anti-alpha-fetoprotein serum on some cultured tumor cells.

Transfer of immunity to Babesia microti of human origin using T lymphocytes in mice.

Summary The cytotoxic potential of heterologous rabbit antibody directed against mouse serum albumin (MSA) and α-fetoprotein (AFP) was investigated in vitro with a cell line (Hepa) derived from the mouse hepatoma BW7756. Anti-AFP in the presence of complement could kill Hepa cells at concentrations of anti-MSA that were virtually nontoxic. The specificity of the anti-AFP was defined by demonstrating that Hepa cell toxicity was dependent upon and paralleled the secretion of AFP in synchronized cultures. Furthermore, neither antiserum could be shown to be significantly toxic to mouse neuroblastoma cells (Neuro-2A). Immunoglobulin purified from pools of antisera was also highly effective in producing cytotoxicity even in a complement-free system. This reaction proceeded more slowly, requiring nearly 48 hr to reach maximum effect in comparison to the 12 hr for complement-mediated toxicity. MSA and AFP are secreted during different phases of the cell cycle. In cultures arrested by isoleucine starvation, labeled AFP appears in the medium 10 hr after release of the blockade in association with S phase. The appearance of labeled MSA is delayed until the first mitosis. Cytotoxic effects of anti-AFP parallel the secretion of AFP in synchronous cultures. Both antisera could be inhibitory to the secretion and synthesis of the proteins of their antigenic specificity. MSA synthesis was more susceptible to this inhibition than was AFP synthesis. The significance of this phenomenon and its association with the differential cytotoxicity of the antiserum are discussed.

The Influence of Antisera Specific for α-Fetoprotein and Mouse Serum Albumin on the Viability and Protein Synthesis of Cultured Mouse Hepatoma Cells

Goat and rabbit anti-mouse IgG were significantly cytotoxic for adult mouse lymphocytes from spleen, lymph node, peripheral blood, and to a lesser extent, bone marrow. Newborn mouse spleen lymphocytes were not susceptible to this cytotoxic effect, but spleen lymphocytes from 1 week old and 1 month old donors were increasingly so. Absorption of anti-mouse IgG sera with mouse spleen cells or mouse IgG removed both IgG precipitins and lymphocytotoxins. Absorption with mouse red cells or foetal tissue, however, did not remove either cytotoxins or IgG precipitins. Antisera directed against human or rabbit IgG's were not cytotoxic for human or rabbit peripheral blood lymphocytes.

The cytotoxic effect of heterologous antisera to mouse IgG on mouse lymphocytes.

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The cytotoxic effect of heterologous antisera to mouse IgG on mouse lymphocytes.