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Biomedical subjects

H Waldmann

Publications and source records attributed to H Waldmann.

At least 379 records · Page 21Linked to original sources
PubMed1975

The failure to show a necessary role for C3 in the in vitro antibody response.

The in vitro antibody response of mouse spleen cells to TNP coupled to both T-dependent and T-independent carriers as well as to sheep erythrocytes has been studied to investigate the possible role of complement activation in the induction of antibody formation. The following has been found. (1) In vitro responses of both IgM and IgG can be obtained to both T-dependent and T-independent antigens in serum-free media, although they are smaller than those found in serum-containing media. This shows that no exogenous source of complement is necessary for in vitro antibody formation by spleen cells. (2) Similarly, normal antibody responses are obtained if the cultures are grown in human serum depleted of C3b-inactivator, which contains high concentrations of C3b. (3) In the presence of antibody to mouse C3 the response to the T-independent antigen is reduced, the IgM responses being more affected than the IgG. However, purified F(ab')2 anti-C3 has no inhibitory effect and it therefore seems likely that it is the formation of intact immune complexes containing Fc rather than the interference with C3 function that is responsible for the inhibition seen. (4) The conventionally purified anti-complementary factor from cobra venom has no effect on the antibody response in serum-free culture or when human or fetal calf sera are used. In no experiment was any potentiation of T-dependent responses observed. However, the presence of quite small concentrations (2%) of cobra veno

Animals↗
PubMed1975

Limiting dilution analysis of helper T-cell function.

Limiting dilution analysis has been applied to the study of T-cell 'helper' function in vitro. Using the microculture system one can estimate the numbers of (a) 'helper' T cells involved in specific collaboration with B cells and (b) those T cells which are able, on being activated by their specific antigen, to facilitate the response of B cells to another antigen. Such studies have enabled us to demonstrate that: (1) a single 'helper' T cell was able to activate a single B-cell precursor to detectable antibody production; (2) the 'helper' function of primed T cells was radio-resistant; (3) a minimal estimate of 'helper' frequencies could be obtained in defined cell populations; (4) nonspecific facilitation was directed towards virtually all available B cells of a given specificity if these were challenged with their appropriate particulate antigen; (5) the microculture system offers the opportunity to determine whether specific and non-specific T-cell 'helper' effects are a consequence of the activity of one T-cell type or of differenct subpopulations of T cells.

Animals↗
PubMed1975

T cell-dependent mediator in the immune response. III. The role of non-specific factor (NSF) in the in vitro immune response.

Evidence is presented which suggests that T cell-dependent nonspecific factor (NSF) cannot be the sole mediator of 'co-operation' for all types of thymus-dependent antibody response. NSF can replace the requirement for T cells in responses to hapten conjugated to particulate carriers, but cannot do so in responses to hapten conjugates of soluble thymus-dependent carriers.

Animals↗
PubMed1975

The inter-relationship of antigenic structure, thymus-independence and adjuvanticity. IV. A general model for B-cell induction.

Polymerized flagellin and E. coli lipopolysaccharide both express adjuvanticity in vivo and in vitro for responses to hapten conjugated to sheep erythrocytes, and hapten conjugated to soluble thymus-dependent antigens. In the case of erythrocyte-bound hapten, adjuvanticity is expressed in the absence of thymus-derived cells (T cells). However, in the case of responses to soluble thymus-dependent conjugates, carrier-specific T cells would appear to be necessary for adjuvanticity to be expressed. On the basis of these observations an hypothesis for the mechanism of B-cell induction and tolerance is proposed.

Adjuvants, Immunologic↗
PubMed1975

T cell-dependent mediator and B-cell clones.

Supernatants were collected from keyhole limpet haemocyanin (KLH) primed spleen cells which had been incubated in tissue culture medium with their priming antigen KLH. These non-specific factor (NSF) containing supernatants were then tested in a microculture system for their ability to facilitate an anti-SRBC response of nu/nu or AT times BM spleen cells. It was concluded that:(a) NSF was able to engage a large number of the available pool of sheep erythrocyte (SRBC) specific B cells into an antibody response (b) this response was characterized by the development of clones expressing plaque-forming cells (PFC), the number of PFC produced within a clone being dependent upon the amount of NSF available in that culture; (c) NSF probably acted directly on B cells, and not via other accessory cell types.

Adjuvants, Immunologic↗
PubMed1975

The 'intrinsic adjuvanticity' and immunogenicity of trinitrophenylated lipopolysaccharide.

One thymus-independent immunogen, trinitrophenylated lipopolysaccharide (TNP-LPS) has been studied in vivo and in vitro in C3H/He and C3H/HeJ strains of mice. C3H/HeJ mice have been shown to be low responders, and C3H/He mice high responders to this immunogen. This 'low responder' status of C3H/HeJ mice has been demonstrated to be consequent to an intrinsic defect present at least at the level of B cells. It was demonstrated that high responder cells or 'in vivo milieu' could not restore this deficit to C3H/HeJ cells. It is proposed that the adjuvanticity, mitogenicity and polyclonal activating capacity of LPS are all fundamental to its property of acting as a thymus-independent carrier for the TNP determinant. This observation is discussed from the point of view that the T-cell independence for an antigen cannot derive solely from its multivalency but must depend upon the intrinsic adjuvanticity of that molecule.

Adjuvants, Immunologic↗