The influence of the H-2 complex on responses to infection by Schistosoma mansoni in mice

Parasitology ◽  
1983 ◽  
Vol 86 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Janet T. Jones ◽  
D. M. Mccaffery ◽  
J. R. Kusel

SUMMARYIn order to determine whether a given H-2 haplotype has similar effects on responses to schistosomiasis mansoni on different genetic backgrounds, mice of 2 pairs of congenic strains (H-2b and H-2k on BALB/c and C57BL/10 backgrounds) were infected. Worm burdens, mortality, splenomegaly, tissue and faecal egg counts, and antibody titres to worm and egg antigens were measured. The genetic background had a major effect on the genesis of splenomegaly, on the deposition of eggs in the spleen, the maximum faecal egg count, the antibody titre to egg and worm antigens and the rate of generation of antibody response. The H-2 haplotype was shown to consistently influence the maximum faecal egg count and the antibody titres. Worm burden was not influenced by genetic differences between strains and mortality differences were not significant. The data presented here indicate that the effect of the major histocompatibility complex on responses to infection is greatly influenced by the genetic background on which it is expressed.

2020 ◽  
Vol 99 (10) ◽  
pp. 4804-4808
Author(s):  
N.G. Wilkinson ◽  
R.T. Kopulos ◽  
L.M. Yates ◽  
W.E. Briles ◽  
R.L. Taylor

1995 ◽  
Vol 37 (4) ◽  
pp. 325-329 ◽  
Author(s):  
Regina Lunardi Rocha ◽  
Manoel Otávio da Costa Rocha ◽  
Ênio Roberto Pietra Pedroso ◽  
Enrico Antônio Colosimo ◽  
Paulo Marcos Zech Coelho

Stability of faecal egg excretion and correlation with results related to worm burden at the initial phase of schistosomiasis mansoni were observed in two groups of mice infected with different Schistosoma mansoni cercarial burdens, by means of analysis of quantitative parasitological studies and schistosome counts after perfusion. Thus, it may be stated that few quantitative parasitological stool examinations could be sufficient to express the infection intensity at the initial phase, on the same grounds that it was already demonstrated at the chronic phase. Furthermore, it is confirmed that the use of the number of eggs passed in the faeces as a tool to estimate the worm burden at the initial phase of schistosome infection is adequate.


Development ◽  
1984 ◽  
Vol 84 (1) ◽  
pp. 287-302
Author(s):  
A. J. H. Gearing ◽  
Frances A. Cribbin ◽  
J. D. Horton

These experiments make use of an amphibian model system for investigating the role of the thymus in T helper cell education. Clawed toads (Xenopus laevis), thymectomized at 7 days, are unable to mount an antibody response to thymus-dependent antigens, such as sheep red blood cells (SRBC). When thymectomized larvae are implanted with larval thymuses (either irradiated or non-irradiated), incompatible at the major histocompatibility complex (MHC) or with MHC-compatible or -incompatible ‘adult’ thymuses, their splenic plaque-forming cell response and serum haemolytic antibody production to SRBC are both restored, to some extent. However, levels of mercaptoethanol-resistant antibody were extremely poor in those animals implanted with MHC-incompatible ‘adult’ thymus. Larval thymus implants were shown, by ploidy-labelling studies, to become repopulated with host-derived lymphocytes. Whether or not these lymphocytes acquire their MHC restriction specificities in the thymus awaits clarification.


1982 ◽  
Vol 155 (1) ◽  
pp. 303-320 ◽  
Author(s):  
G W Butcher ◽  
J R Corvalán ◽  
D R Licence ◽  
J C Howard

We have identified two major histocompatibility complex (MHC)-linked Ir genes that control the antibody response made by rats against class I major alloantigens. We have named these genes Ir-RT1Aa and Ir-RT1Ac. These Ir genes determine responsiveness of the immunized animal in a typical codominant fashion. There is no evidence so far for trans-complementation between low-responder haplotypes. Detailed studies of Ir-RT1Aa indicate that it controls the antibody response to at least two distinct alloantigenic determinants on RT1Aa molecules. These class I molecules thus behave like hapten-carrier conjugates when the response against the carrier is under Ir gene control. Analysis of the origin of alloantibody-forming cells in tetraparental radiation chimeras indicates that Ir-RT1Aa must control the provision of effective help to B cells. In many respects therefore, the properties of Ir-RT1Aa are broadly similar to those described for Ir genes controlling antibody responses to conventional antigens. The existence of apparently conventional Ir genes controlling the antibody response to major alloantigens strongly suggest that the processing of these transmembrane molecules by host antigen-presenting cells is a prerequisite for immune induction, and that it is the MHC of the responder rather than that of the allograft to which T helper cells are restricted in alloimmune responses in vivo.


Parasitology ◽  
1989 ◽  
Vol 99 (3) ◽  
pp. 357-364
Author(s):  
V. S. Delgado ◽  
D. J. Mclaren

SummaryNaive CBA/Ca mice and CBA/Ca mice infected 12 weeks previously with 20 normal cercariae of Schistosoma mansoni were challenged percutaneously with isotopically labelled parasites. Challenge worm migration was followed, in 5 separate experiments, by means of compressed organ autoradiography. In three experiments, 43.1 % of challenge parasites did not arrive in the lungs of infected mice on day 6 as compared to 7.7 % in naive controls, thereby indicating that pre-lung sites constitute the first barrier in resistance to reinfection. A further 15% of the challenge worm burden was lost in the lungs or en route to the liver in the immune animals, and portal perfusion revealed that 25.4% of the challenge was lost in the liver. Two other experiments revealed no comparable phases of pre-liver attrition however; instead resistance was only evident at final perfusion on days 28 or 35. These data reveal the variable generation of specific acquired immunity in mice harbouring a chronic schistosome infection and thus clarify current discrepancies in the literature. The results are discussed in relation to documented evidence for the nature of specific and non-specific immune mechanisms reported to operate at different sites in the infection model of schistosomiasis mansoni.


2003 ◽  
Vol 77 (10) ◽  
pp. 6076-6081 ◽  
Author(s):  
Yoshio Hashimoto ◽  
Horng-Shen Chen ◽  
Cynthia Cunningham ◽  
Tahir H. Malik ◽  
Patrick K. Lai

ABSTRACT Borna disease virus (BDV) infection of Lewis rats is the most studied animal model of Borna disease, an often fatal encephalomyelitis. In this experimental model, BDV-specific CD8+ cytotoxic T lymphocytes (CTLs) play a prominent role in the immunopathogenesis of infection by the noncytolytic, persistent BDV. Of the six open reading frames of BDV, CTLs to BDV X (p10) and the l-polymerase have never been studied. In this study, we used plasmid immunization to investigate the CTL response to BDV X and N. Plasmid-based immunization was a potent CTL inducer in Lewis rats. Anti-X CTLs were primed by a single injection of the p10 cDNA. Two codominant p10 epitopes, M1SSDLRLTLL10 and T8LLELVRRL16, associated with the RT1.Al major histocompatibility complex class I molecules of the Lewis rats, were identified. In addition, immunization with a BDV p40-expressing plasmid confirmed the previously reported RT1.Al-restricted A230SYAQMTTY238 peptide as the CTL target for BDV N. In contrast to the CTL responses, plasmid vaccination was a poor inducer of an antibody response to p10. Three injections of a recombinant eukaryotic expression plasmid of BDV p10 were needed to generate a weak anti-p10 immunoglobulin M response. However, the antibody response could be optimized by a protein boost after priming with cDNA.


2001 ◽  
Vol 69 (3) ◽  
pp. 1708-1713 ◽  
Author(s):  
Vijaya Nagabhushanam ◽  
Christina Cheers

ABSTRACT Infection of different strains of mice withMycobacterium avium has revealed genetic control of the immunoglobulin isotype induced and of the balance between Th1 and Th2 cytokines. Female BALB/c or C57BL/10 mice were infected intranasally with 105 M. avium organisms. The antibody response was measured over 18 weeks by enzyme-linked immunosorbent assay and Western blotting, while numbers of cytokine-producing cells were assessed at 12 to 15 weeks by ELISPOT assay. Upon infection, C57BL/10 mice produced a clear Th1 response with strong gamma interferon (IFN-γ) production, no interleukin-4 (IL-4), and almost entirely immunoglobulin G2a (IgG2a) antibody. In contrast, BALB/c mice developed T cells producing IL-4, as well as those producing IFN-γ, while the antibody response was a mixture of IgG1 and IgG2a. Antibodies from BALB/c mice were also able to recognize a greater range of antigens than were C56BL/10 mice. B10D2 mice, which carry the BALB/c major histocompatibility complex haplotype on a C57BL/10 background, followed the C57BL/10 cytokine pattern. Mice infected withListeria monocytogenes did not show a similar response dichotomy.


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