scholarly journals Sharing of Ia antigens between species. I. Detection of Ia specificities shared by rats and mice.

1977 ◽  
Vol 146 (2) ◽  
pp. 381-393 ◽  
Author(s):  
D H Sachs ◽  
G W Humphrey ◽  
J K Lunney

A mouse anti-rat xenogeneic antiserum, B10.D2 anti-BN, has been found to react with a subpopulation of lymphoid cells of certain mouse strains. The corresponding alloantiserum, B10.D2 anti-B10.BR, reacted in analogous fashion with lymphoid cells of BN rats. In the case of the cross-reaction on mouse cells, mapping studies indicated that at least part of the reactivity was with the product of gene(s) determined by the I-A subregion of the H-2 complex. Chemical isolation studies with radiolabeled cell surface preparations indicated that the antigens detected in both mouse and rat had mol wt characteristic of Ia antigens (35,000 and 28,000 dalton molecules). Testing of fractionated spleen cell populations revealed that the cross-reactive antigens were expressed predominatly on B cells, but that a subpopulation of T cells were also reactive. Wider strain and species distribution studies are in progress to determine the extent of such Ia cross-reactions between species and to further assess the practical and theoretical importance of such cross-reactions.

1977 ◽  
Vol 145 (2) ◽  
pp. 327-343 ◽  
Author(s):  
R H Schwartz ◽  
C L Horton ◽  
W E Paul

Antibodies raised against many structurally related antigens have been shown to cross-react extensively. Manifestations of T-cell immunity, on the other hand, appear to be more restricted in their ability to be elicited by cross-reacting antigens, although examples have been reported. This paper explores the nature of the cross-reactions at the T-cell level among the branched-chain copolymers (T,G)-A--L, (phi,G)-A--L, (H,G)-A--L, and G-A--L, as well as a related linear terpolymer, GAT, in a variety of mouse strains using the peritoneal exudate T-lymphocyte-enriched cells (PETLES) proliferation assay. (T,G)-A--L, (phi,G)-A--L, and GAT could cross-stimulate cells immune to the other two antigens, whereas (H,G)-A--L, (T,G)-Pro--L, and G-A--L showed no cross-stimulations. The extent of the cross-reactions varied with the mouse strain and was shown to be under the control of immune response genes. It was necessary for the strain to be able to respond to both the immunogen and the cross-reacting antigen, when used as an immunogen, in order for cross-stimulation to occur; however, this was not always sufficient. Several examples of unequal or one-way cross-reactions were found. In addition, the immune responses to (H,G)-A--L and (phi,G)-A--L showed no cross-reactions with the other antigen even though their Ir genes were both mapped to the K region or I-A subregion. The problem of accounting for such fine specificity of T-cell recognition in lieu of the genetic evidence demonstrating only Ir gene control of the response is discussed.


1981 ◽  
Vol 2 (2) ◽  
pp. 113-123 ◽  
Author(s):  
H.A. Vaughan ◽  
M.S. Sandrin ◽  
I.F.C. McKenzie ◽  
B.D. Tait ◽  
A. Ting
Keyword(s):  

1982 ◽  
Vol 156 (3) ◽  
pp. 860-872 ◽  
Author(s):  
S B Binion ◽  
L S Rodkey

Naturally induced auto-anti-idiotypic (AAI) antibody responses specific for antimicrococcal antibody idiotypes were detected in 42% of the rabbits in a family immunized with Micrococcus lysodeikticus. The natural AAI response of each rabbit recognized only a portion (11-41%) of that individual's total antimicrococcal antibody population. Cross-reactions of idiotypes were observed within the group of rabbits exhibiting natural AAI responses. Examination of the basis for the cross-reactions showed that the natural AAI antisera recognized identical idiotopes on the antimicrococcal F(ab')2 fragments from each rabbit that made an AAI response. The cross-reactive idiotopes were shown to be of paternal origin and were found in the antimicrococcal antibodies of each offspring. The data strongly support the idiotypic network concept that naturally induced AAI responses may occur routinely in outbred normal individuals as a result of antigenic stimulation. Further, the data suggest that the induction of regulatory AAI antibody responses in outbred rabbits may depend on the expression of particular germ line idiotopes.


1970 ◽  
Vol 131 (2) ◽  
pp. 223-234 ◽  
Author(s):  
Harvey Cantor ◽  
Richard Asofsky ◽  
Norman Talal

The ability of spleen cells from young (3 month) and old (1 yr) NZB mice to induce GVH reactions in newborn C57BL/6N mice was compared quantitatively using the Simonsen spleen assay. Young NZB cells were five times more reactive than cells from older mice. The minimum number of cells producing detectable reactions was 2 x 106 for the young and 10 x 106 for the old. Young and old cells combined and injected together produced GVH reactions quantitatively similar to those obtained with inocula composed of young cells alone. Mixtures of two cell populations producing no detectable reactions when injected separately into different recipients (1 x 106 young cells and 4 x 106 old cells) produced reactions approximately equal to those obtained with 5 x 106 young cells. As few as 0.25 x 106 young cells were sufficient to effect a reaction when combined with 4.75 x 106 old unreactive cells. Viability of both cell populations was essential for GVH reactivity. This evidence of synergy in GVH reactions indicates that old NZB spleen cells can be rendered immunologically more reactive in the presence of a normally reactive population.


2021 ◽  
Author(s):  
Brea K Hampton ◽  
Kara L. Jensen ◽  
Alan C. Whitmore ◽  
Colton L. Linnertz ◽  
Paul Maurizio ◽  
...  

Variation in immune homeostasis, immune system stability, in organ systems such as the lungs is likely to shape the host response to infection at these exposed tissues. We evaluated immune homeostasis in immune cell populations in the lungs of the Collaborative Cross (CC) mouse genetic reference population. We found vast heritable variation in leukocyte populations with the frequency of many of these cell types showing distinct patterns relative to classic inbred strains C57BL/6J and BALB/cJ. We identified 28 quantitative trait loci (QTL) associated with variation in baseline lung immune cell populations, including several loci that broadly regulate the abundance of immune populations from distinct developmental lineages, and found that many of these loci have predictive value for influenza disease outcomes, demonstrating that genetic determinants of homeostatic immunity in the lungs regulate susceptibility to virus-induced disease. All told, we highlight the need to assess diverse mouse strains in understanding immune homeostasis and resulting immune responses.


Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2422-2430 ◽  
Author(s):  
FC Zeigler ◽  
BD Bennett ◽  
CT Jordan ◽  
SD Spencer ◽  
S Baumhueter ◽  
...  

The flk-2/flt-3 receptor tyrosine kinase was cloned from a hematopoietic stem cell population and is considered to play a potential role in the developmental fate of the stem cell. Using antibodies derived against the extracellular domain of the receptor, we show that stem cells from both murine fetal liver and bone marrow can express flk-2/flt-3. However, in both these tissues, there are stem cell populations that do not express the receptor. Cell cycle analysis shows that stem cells that do not express the receptor have a greater percentage of the population in G0 when compared with the flk-2/flt-3- positive population. Development of agonist antibodies to the receptor shows a proliferative role for the receptor in stem cell populations. Stimulation with an agonist antibody gives rise to an expansion of both myeloid and lymphoid cells and this effect is enhanced by the addition of kit ligand. These studies serve to further illustrate the importance of the flk-2/flt-3 receptor in the regulation of the hematopoietic stem cell.


2021 ◽  
Author(s):  
Clare M. Williams ◽  
Sreeja Roy ◽  
Danielle Califano ◽  
Andrew N. J. McKenzie ◽  
Dennis W. Metzger ◽  
...  

Interleukin (IL)-33 is a multifunctional cytokine that mediates type 2 dominated immune responses. In contrast, the role of IL-33 during viral vaccination, which often aims to induce type 1 immunity, has not been fully investigated. Here we examined the effects of IL-33 on influenza vaccine responses. We found that intranasal co-administration of IL-33 with an inactivated influenza virus vaccine increases the vaccine efficacy against influenza infection, not only with the homologous strain, but also heterologous strains including the 2009 H1N1 influenza pandemic strain. The cross-protection was dependent on group 2 innate lymphoid cells (ILC2s), as the beneficial effect of IL-33 on vaccine efficacy was abrogated in ILC2-deficient C57BL/6 Il7r P Cre/+ P Rora P fl/fl P mice. Further, mechanistic studies revealed that IL-33 activated ILC2s potentiate vaccine efficacy by enhancing mucosal humoral immunity, particularly IgA responses, potentially via a Th2 cytokine dependent manner. Our results demonstrate that IL-33-mediated activation of ILC2s is a critical early event that is important for the induction of mucosal humoral immunity, which in turn is responsible for cross-strain protection against influenza. Thus, we reveal a previously unrecognized role for the IL-33/ILC2 axis in establishing broadly protective and long-lasting humoral mucosal immunity against influenza – knowledge that may help develop a universal influenza vaccine. Importance Current influenza vaccines, although capable of protecting against predicted viruses/strains included in the vaccine, are inept at providing cross-protection against emerging/novel strains. Thus, we are in critical need for a universal vaccine that can protect against a wide range of influenza viruses. Our novel findings show that a mucosal vaccination strategy involving the activation of lung ILC2s is highly effective in eliciting cross-protective humoral immunity in the lungs. This suggests that the biology of lung ILC2s can be exploited to increase the cross-reactivity of commercially available influenza subunit vaccines.


Vox Sanguinis ◽  
1982 ◽  
Vol 43 (1) ◽  
pp. 1-10
Author(s):  
Marilyn S. Pollack ◽  
Mary N. Crawford ◽  
Harriet M. Robinson ◽  
Rachel Berger ◽  
Bernice Sabo ◽  
...  
Keyword(s):  

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