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Interestingly, incidence of HCMV transmission and severity of the associated morbidities seem to be reduced during recurrent episodes compared to primary infections [6] [8], indicating that the adaptive immune response is capable to mediate some protection to the foetus.
Importantly, this DENV-specific humoral response is capable of preventing infection by neutralizing virus of the infecting serotype only.
These observations provide evidence that the human immune response is capable of controlling coordinated global HIV-1 reactivation, remarkably with potency equivalent to combination antiretroviral therapy.
We combined in vivo, in silico, and in vitro approaches to demonstrate for the first time that the human immune response is capable of controlling an iatrogenic large-scale HIV-1 reactivation, as might be induced by LRAs.
Given the biological and immunological complexity of the P. falciparum blood-stage, it seems likely that more than one immunological response is capable of contributing to protection and therefore unlikely that a single assay will predict all mechanisms of blood-stage immunity.
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We therefore hypothesized that the mammalian systemic inflammatory response was capable of causing IEC apoptosis and shedding at the villus tip when triggered by LPS, and that this occurred prior to the onset of apoptosis in the crypt.
These data demonstrate that the non-immunogenic, ES2 (in terms of eliciting 2F5 epitope-specific responses), is capable of effectively driving 2F5 epitope-specific memory B cell responses if effectively primed.
For example, in animals that are sensitized to ova albumin and infected with M. pneumoniae, airway remodeling can be observed suggesting that M. pneumoniae mediated inflammatory responses are capable of causing long-term lung damage [10].
Although we report the presence of anti-tumor antibodies produced by patient memory B cells, and these cells were stimulated ex vivo to secrete antibodies, it is not clear whether tumor antigen-reactive B cells are activated in patients to secrete antibodies or whether these humoral responses are capable of exerting any beneficial anti-tumoral activities in the same patients in vivo.
100 Host immune responses are capable of suppressing tumors.
Further studies are necessary to determine which system responses are capable of rapid recovery or slower re-establishment of native feedback loops and whether patterns of responses are similar across differing environments.
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