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Biomedical subjects

N K Jerne

Publications and source records attributed to N K Jerne.

At least 19 recordsLinked to original sources
PubMed1984

Idiotypic networks and other preconceived ideas.

The preceding section implies that the immune system (like the brain) reflects first ourselves, then produces a reflection of this reflection, and that subsequently it reflects the outside world: a hall of mirrors. The second mirror images (i.e., stable anti-idiotypic elements) may well be more complex than the first images (i.e., anti-self). Both give rise to distortions (e.g., mutations, gene rearrangements) permitting the recognition of nonself. The mirror images of the outside world, however, do not have permanency in the genome. Every individual must start with self. Paraphrasing Nicolas Schöffer (Schöffer 1982): those who always seek exterior pressures (e.g., microbes) to account for the evolution of the sets of V genes, would do well to turn their vision towards the interiors of themselves, and there discover the mystery, perhaps never completely revealable, of the immune system.

Animals↗
PubMed1982

Recurrent idiotopes and internal images.

A rabbit was immunized with rabbit immunoglobulins of a different allotype. The anti-allotypic antibodies produced by this rabbit were used to immunize a second rabbit which produced anti-idiotypic antibodies. To explain the occurrence, among these anti-idiotypic antibodies, of "internal images" of the original immunizing allotype, a restricted and a more general hypothesis are developed. The first assumes that B-cells can be triggered when idiotopes on their receptor molecules are recognized by the paratopes of the immunizing antibody. The second denies the existence of a specially constructed combining site on the variable domain of an antibody molecule.

Animals↗
PubMed1980

IgM antibodies induce the production of antibodies of the same specificity.

Injection in normal mice of IgM antibodies against sheep erythrocytes or dextran, in the form of an immune serum depleted og IgG, induces direct plaque-forming cells of the same specificity as the injected antibodies. The response is 10--70 times higher than the background plaque-forming cell titer of untreated control mice. Nanogram amounts of IgM induce a detectable response, and a ceiling is reached with a few hundred nanograms of monoclonal IgM. The inducing agent is not residual antigen: (i) treatment of the injected material and the recipients with dextranase abolishes the immunogenicity of dextran, but not the response to anti-dextran IgM; (ii) monoclonal IgM specific for sheep erythrocytes or trinitrophenyl likewise induces plaque-forming cells of the respective specificity, but variant hybridoma products (in which the light chain is that of the myeloma parent) are inactive. In normal mice, IgM-induced antibody responses were observed with antibodies to both thymus-dependent and thymus-independent antigens, but such could not be induced in athymic (nude) mice. Because the mechanism underlying this phenomenon would operate also in a normal immune response and, presumably, in the normal dynamic state of the immune system of unstimulated animals, a network regulation among the elements of the immune system itself is implied.

Animals↗
PubMed1978

Major histocompatibility complex-linked immune-responsiveness is acquired by lymphocytes of low-responder mice differentiating in thymus of high-responder mice.

Female murine T cells can respond to the Y antigen of male cells by generating cytotoxic T-killer lymphocytes. Responsiveness is linked to several H-2 genes. Two types of low responders can be distinguished: the B10.A(5R) (H-2i5) strain, a low responder because it lacks Y-specific precursor T cells able to differentiate into cytotoxic T-killer cells; and the CBA/J (H-2k) strain, a low responder because it lacks Y-specific T-helper cells able to support differentiation of T-killer cell precursors. B10.A(5R) stem cells differentiating in an x-irradiated (CBA/J X C57BL/6) (H-2k X H-2b)F1 host respond to Y antigen by generating T-killer cells whereas CBA/J stem cells do not. The results are consistent with the hypothesis that diversity of T-cell receptors is generated by somatic mutation of germ-line genes encoding specificity for self-H-2. A detailed account of this hypothesis is presented.

Animals↗
PubMed1973

The immune system.

Explore the source record for details and available documents.

Antibody Formation↗
PubMed1969

The requirement of more than one antigenic determinant for immunogenicity.

Rabbits primarily stimulated with a BSA (bovine serum albumin)-sulfanilic acid complex will produce a good secondary response to the sulfanilic acid hapten if the carrier used in the secondary stimulus is again BSA, and not if the secondary carrier is HGG (human gamma globulin). In the latter situation, a good secondary response is obtained, however, if the rabbits are pretreated a few weeks earlier with free HGG. We conclude that the immune stimulus involves the recognition of carrier determinants unrelated to the hapten. As the receptors for recognition of unrelated determinants are probably situated on different cells, we suggest that the immune stimulus leading to antibody formation requires the interaction of two antigen-bridged cells.

Aniline Compounds↗