scholarly journals STUDIES ON HYPERSENSITIVITY

1961 ◽  
Vol 113 (3) ◽  
pp. 571-585 ◽  
Author(s):  
P. G. H. Gell ◽  
B. Benacerraf

In earlier observations with the picryl system, it was concluded that contact sensitivity was a form of delayed (cellular) hypersensitivity to conjugates of sensitizer with autologous proteins indistinguishable in its immunological mechanism from other classical forms of delayed hypersensitivity to proteins. This conclusion has been confirmed and extended with the picryl and chlorbenzoyl chloride systems. 1. It is shown that to induce a state of contact sensitivity, the minimal necessary amounts of hapten are of the same order of magnitude, whether this hapten is conjugated with protein or the free reactive chemical itself. From this, it is evident that contamination of conjugates with small amounts of unreacted sensitizer plays no part in the induction of contact reactivity by the conjugate. With the dinitrophenyl system, no contact sensitivity could be induced by the conjugates used; possible reasons for this discrepancy are discussed. 2. Animals sensitized to contact by homologous conjugate can be completely desensitized by injections of such a conjugate in large amount; a similar injection schedule has no effect on the contact sensitivity of animals sensitized with the free reactive sensitizer. 3. The capacity of heterologous (ovalbumin) conjugates to evoke anti-hapten antibodies is shown to be greater than that of homologous (guinea pig seralbumin) conjugates: the reverse is true of their capacity to induce delayed reactivity. 4. Evidence is brought forward to suggest that in animals sensitized with homologous albumin conjugates, the specificity of the delayed reaction involves more than the hapten alone, even though the carrier protein is non-antigenic on its own. The contrast with the apparent lesser specificity of the antibodies later produced is discussed.

1962 ◽  
Vol 115 (5) ◽  
pp. 1037-1051 ◽  
Author(s):  
P. G. H. Cell ◽  
Arthur M. Silverstein

Further data have been presented showing that the specificity of the delayed hypersensitivity reaction in the guinea pig to hapten-protein conjugates involves to a considerable degree a contribution by the protein carrier. The carrier contribution is such that sensitization to guinea pig albumin-m-azobenzenesulfonate, for example, does not result in cross-reaction with conjugates of the same hapten with unrelated proteins such as ovalbumin or human gamma globulin, nor were cross-reactions observed between conjugates prepared with the same hapten, coupled to the same protein, but by two different chemical routes, such that the point of attachment of the hapten to the protein differed. It thus appears that in this system both hapten and carrier protein are necessary, but that neither alone is in general sufficient to stimulate the delayed sensitive cell. Desensitization experiments with cross-reacting hapten-protein conjugates have suggested the presence of a multiplicity of antigenic determinants participating in the elicitation of the delayed lesion, and of a concomitant development of a heterogeneity of specificities in the population of delayed sensitive cells in the sensitized animal. The data are discussed in terms of the apparent requirement of the delayed sensitivity mechanism for a larger functional antigenic determinant than that required for interaction with circulating antibodies. Some possible explanations for this difference, and some of its consequences, are discussed.


1962 ◽  
Vol 115 (5) ◽  
pp. 1023-1036 ◽  
Author(s):  
B. Benacerraf ◽  
B. B. Levine

The effects of the following parameters on the immunologic specificity of delayed and immediate hypersensitivity reactions were investigated in the guinea pig using the picryl and p-toluenesulfonyl systems: (a) the contribution of the carrier protein, (b) the effect of the number of hapten groups per molecule of the immunizing and challenging antigens, and (c) the effect of interposing a 6 carbon chain (ϵ-aminocaproic acid) between the hapten and its usual attachment to the lysine ϵ-NH2 groups of the carrier protein. It was found that induction of delayed hypersensitivity was accomplished equally well with both lightly and heavily coupled conjugates. Sensitized animals which gave strong delayed reactions to the immunizing conjugate cross-reacted poorly or not at all to (a) conjugates of the same hapten with a different carrier protein, or (b) conjugates differing from the immunizing conjugate by having an ϵ-aminocaproyl chain interposed between hapten and its attachment onto the carrier protein. Animals sensitized with either lightly or heavily substituted conjugates exhibited strong delayed reactions to both conjugates, but more intense reactions to the immunizing conjugate were always observed. In contrast to the marker carrier specificity exhibited by the delayed hypersensitivity reactions, immediate hypersensitivity reactions, (specific precipitation, Arthus, and PCA reactions) could be elicited equally well with hapten conjugates of all carrier proteins, as well as with conjugates containing ϵ-aminocaproyl chains interposed between hapten and the carrier protein, provided the number of hapten groups per molecule conjugate was sufficiently high. Both in inducing antibody response and in provoking immediate hypersensitivity reactions, heavily substituted conjugates were considerably more effective than were lightly substituted conjugates. Alternative explanations for these observed differences in specificity between immediate and delayed hypersensitivity reactions are discussed.


1963 ◽  
Vol 117 (6) ◽  
pp. 909-923 ◽  
Author(s):  
Sidney Leskowitz

Delayed hypersensitivity in guinea pigs was produced by immunization. with a conjugate prepared by coupling diazotized arsanilic acid to polytyrosine. The resulting sensitivity could be demonstrated by skin test with conjugates prepared from a wide variety of tyrosine-containing proteins. Definite but smaller degrees of sensitivity could be induced with conjugates of proteins containing little or no tyrosine. The apparent absence of carrier-specificity is considered to be due to the narrowed range of immunologic response produced by immunization with polytyrosine-azobenzenearsonate. Injections of the hapten N-acetyltyrosine-azobenzenearsonate was found to suppress completely the delayed reaction attributable to the tyrosine-azobenzenearsonate group. The same hapten was only slightly effective in suppressing reactions in guinea pigs immunized with guinea pig serum albumin-azobenzenearsonate, suggesting that a broader range of specificities is involved with such antigens. Confirmation of such increased range of specificity attributable to antigenic determinants contributed by the carrier protein was obtained by desensitization studies with N-acetyltyrosine-azobenzenearsonate and guinea pig serum albumin-azobenzoate. While separately these materials produced only a slight decrease in skin reactivity to guinea pig serum albumin-azobenzenearsonate, the combination was found to give almost complete suppression.


1995 ◽  
Vol 23 (5) ◽  
pp. 295-299 ◽  
Author(s):  
K. Katsuno ◽  
A. Manabe ◽  
K. Itoh ◽  
H. Hisamitsu ◽  
S. Wakumoto ◽  
...  

2013 ◽  
Vol 95 (1) ◽  
pp. e20-e21 ◽  
Author(s):  
RJ Livingston ◽  
JW Butterworth ◽  
P Belt

Chloramphenicol is a topical treatment that is used widely, especially in wounds around the eyes. In our practice there have been a number of cases of delayed hypersensitivity to chloramphenicol that has been mismanaged initially as an infective cellulitis. We hope to share some of our experience of this uncommon reaction to highlight the delayed reaction that can occur with topical application of this drug.


1952 ◽  
Vol 96 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Erwin Neter ◽  
Lee F. Bertram ◽  
Dorothy A. Zak ◽  
Miriam R. Murdock ◽  
Carl E. Arbesman

A study on hemagglutination and hemolysis by Escherichia coli O111 and O55 (rabbit) antisera and on hemagglutination and hemolysis inhibition by E. coli O111 and O55 antigens revealed the following facts. 1. Red blood cells of man, dog, rabbit, guinea pig, sheep, rat, and chicken adsorb E. coli O111 and O55 antigens and thus become specifically agglutinable by the homologous E. coli antisera. 2. The adsorption of these E. coli antigens is a function of the concentration of the antigen, the time (from 5 minutes to 2 hours) of treatment of the red blood cells with the antigen, and the concentration of the red blood cells used. 3. Red blood cells of man and sheep adsorb simultaneously both antigens, as indicated by the fact that both antisera give agglutination of all red blood cells. Complete agglutination does not occur when a mixture of red blood cells treated separately with the two antigens is added to one or the other of the two antisera. 4. Treatment of red blood cells of man with one of the antigens does not block the adsorption of the second antigen. Human cells treated with either or both antigens are still agglutinated by the homologous blood group (A, B, and Rh)-specific antibodies. 5. In the presence of guinea pig complement, E. coli O111 and O55 antisera produce hemolysis of modified human red blood cells in titers of the same order of magnitude as those giving hemagglutination and bacterial agglutination. The same antisera produce hemolysis of sheep cells treated with the identical antigens in titers exceeding by far those giving agglutination of modified human or sheep red blood cells. 6. Both sediment and supernate of a boiled E. coli suspension are capable of modifying red blood cells for E. coli hemagglutination; in contrast, the supernate obtained from an unboiled suspension and then heated does not modify red blood cells for hemagglutination, although it contains the antigen which can specifically adsorb E. coli antibodies, as shown by means of the hemagglutination and hemolysis inhibition tests. 7. Both the unheated and the boiled suspensions of E. coli O111 and O55 inhibit hemagglutination and hemolysis specifically. 8. Rabbit red blood cells modified by either E. coli O111 or 055 antigens, upon intravenous injection into rabbits, engender specific E. coli antibodies. The significance of the results is discussed.


1975 ◽  
Vol 46 (2) ◽  
pp. 90-101 ◽  
Author(s):  
Efrain Peretzman ◽  
Patrick D. Toto ◽  
Anthony W. Gargiulo

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