scholarly journals Neonatal treatment with low doses of anti-idiotypic antibody leads to the expression of a silent clone.

1981 ◽  
Vol 153 (4) ◽  
pp. 1004-1008 ◽  
Author(s):  
J Hiernaux ◽  
C Bona ◽  
P J Baker

BALB/c mice immunized with bacterial levan (BL) produce an immune response that fails to generate antibody expressing the idiotype (Id) of the beta (2 leads to 6) fructosan-binding myeloma protein ABPC 48 (A48). Pretreatment of newborn BALB/c mice (at 1 d of age) with 0.01-10 microgram of affinity purified BALB/c anti-A48 Id antibody followed by immunization with BL 1-2 mo later produces an anti-BL response that expresses the A48 Id. This shows that A48 Id+ anti-BL clones belong to a normally silent fraction of the anti-BL repertoire. The activation of A48 Id+ anti-BL clones anti-A48 Id antibody is specific because the pretreatment of newborn mice with anti-MOPC 384 Id antibody, followed by immunization with BL, does not lead to its activation. Moreover, pretreatment of mice with anti-A48 Id antibody does not alter the MOPC 460 Id+ component of the anti-TNP response. It is also important to note that the activation of the A48 Id+ clone in pretreated mice requires subsequent immunization with BL.

2012 ◽  
Vol 279 (1746) ◽  
pp. 4505-4512 ◽  
Author(s):  
Hannah J. Tidbury ◽  
Alex Best ◽  
Mike Boots

Exposure to low doses of pathogens that do not result in the host becoming infectious may ‘prime’ the immune response and increase protection to subsequent challenge. There is increasing evidence that such immune priming is a widespread and important feature of invertebrate host–pathogen interactions. Immune priming clearly has implications for individual hosts but will also have population-level implications. We present a susceptible–primed–infectious model—in contrast to the classic susceptible–infectious–recovered framework—to investigate the impacts of immune priming on pathogen persistence and population stability. We describe impacts of immune priming on the epidemiology of the disease in both constant and seasonal environments. A key result is that immune priming may act to destabilize population dynamics. In particular, when the proportion of individuals becoming primed rather than infected is high, but this priming does not confer full immunity, the population may be strongly destabilized through the generation of limit cycles. We discuss the implications of our model both in the context of invertebrate immunity and more widely.


1986 ◽  
Vol 101 (1) ◽  
pp. 93-104 ◽  
Author(s):  
B.S. Bhogal ◽  
Y.D. Karkhanis ◽  
M.K. Bell ◽  
P. Sanchez ◽  
B. Zemcik ◽  
...  

1977 ◽  
Vol 21 (6) ◽  
pp. 685-690 ◽  
Author(s):  
Ramesh D. Kulkarni ◽  
Lexley M. DaSilva ◽  
Nari L. Chabria ◽  
Dev R. Chadha
Keyword(s):  

1985 ◽  
Vol 94 (2) ◽  
pp. 512-520 ◽  
Author(s):  
Gillian M. Shepherd ◽  
Jay J. Gibbons ◽  
Gregory W. Siskind ◽  
G.Jeanette Thorbecke ◽  
Edmond A. Goidl

1997 ◽  
Vol 10 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Kevan C. Herold ◽  
Elizabeth Baumann ◽  
Vaiva Vezys ◽  
Frank Buckingham
Keyword(s):  

1976 ◽  
Vol 143 (4) ◽  
pp. 846-860 ◽  
Author(s):  
S J Black ◽  
G J Hämmerling ◽  
C Berek ◽  
K Rajewsky ◽  
K Eichmann

Guinea pig anti-idiotypic antibodies (anti-Id) of the IgG1 class, directed to an A/J antibody to Group A streptococcal carbohydrate (A-CHO), or directed to a BALB/c myeloma protein that binds the same antigen, stimulate B-precursor cells as well as T-helper cells when injected into mice of the appropriate strain. The strain-specific induction of both precursor and helper activity was detected by in vitro secondary responses of primed spleen cells to A-CHO or to 2,4,6-trinitrophenyl (TNP) upon challenge with Group A streptococcal vaccine (Strep.A) or with TNP-Strep.A, respectively. B- and T-cell populations primed with anti-Id were uniform with respect to the binding of antigen and of anti-Id. This was in contrast to cells primed with Strep.A, which were heterogenous. Taken together, B and T cells that possess the same antigen-binding specificity share idiotypic determinants, reveal the same idiotypic polymorphism, and may display similar degrees of heterogeneity with respect to the binding of antigen and anti-Id. Since the anti-Id used in this study detect Id determinants associated with the heavy chain of the variable region of mouse antibodies, the data suggest that this region of the immunoglobulin molecule is shared between T- and B-cell antigen receptors.


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