Early Interactions Between Blood-Stage Plasmodium Parasites and the Immune System

Author(s):  
B. C. Urban ◽  
R. Ing ◽  
M. M. Stevenson
Keyword(s):  
2000 ◽  
Vol 68 (3) ◽  
pp. 1485-1490 ◽  
Author(s):  
Helena Helmby ◽  
Gun Jönsson ◽  
Marita Troye-Blomberg

ABSTRACT Infection with blood-stage Plasmodium chabaudi chabaudiAS results in splenomegaly, peripheral leukocytosis, and a major activation of the immune system. The frequencies and absolute numbers of T-cell, B-cell, and macrophage populations in spleen and peripheral blood from P. chabaudi-infected BALB/c mice were compared and found to be significantly altered during acute infection. The kinetics of the redistribution of the different cell types in spleen and peripheral blood were different, with T and B cells appearing in the blood when their frequencies and absolute numbers in the spleen were low. The frequency and absolute number of apoptotic cells in the spleen were increased during acute P. chabaudi infection and involved both T cells, B cells, and macrophages. Both Fas and Fas-ligand expression were increased in the spleen. Taken together, our data provide new information on the complex cellular interactions that take place in the immune system during blood-stage malaria infection in a mouse model.


Parasitology ◽  
1989 ◽  
Vol 98 (2) ◽  
pp. 315-327 ◽  
Author(s):  
G. A. Butcher

SUMMARYResistance developed by the immune system in response to blood-stage malaria is complex in nature, involving humoral and non-antibody effector mechnisms. Different species of malarial parasites may vary in their ability to elicit, or their susceptibility to, those immune effectors. This complexity is enhanced by the different results obtained in vaccinated as opposed to drug-controlled infections. It is therefore important that some attempt be made to unravel these interactions. This is particularly so when we have to decide on methods for assessing the potentiality of antigens to induce protective immunity. In this review the limitations of somein vitroassays of immunity, as well as those of various host–parasite models, are discussed. The relative importance of cell-mediated and humoral immunity in laboratory models and natural infections is also considered in the context of vaccine development.


2014 ◽  
Vol 5 ◽  
Author(s):  
Frank Wunderlich ◽  
Saleh Al-Quraishy ◽  
Mohamed A. Dkhil

2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.


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