Tumor Exosomes Make microRNAs
Cellular blebs shed by tumor cells can process short stretches of RNA that go on to induce tumor formation in neighboring cells.
WIKIMEDIA, NATIONAL CANCER INSTITUTE |
An Education Web Page
Why we need to terminate Ebola 2014 before the virus learns too much about us.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
WIKIMEDIA, NATIONAL CANCER INSTITUTE |
Figure 4: Important immune cells in each phase of renal IRI.
Neutrophils and NK T cells infiltrate the post-ischaemic kidney in the early injury phase and contribute to initiation of the inflammatory cascade. NK cells also contribute to renal tissue injury in the early injury phase. Renal dendritic cells increase in number and are activated to mediate inflammation from the early to late injury phase. Macrophages have diverse roles throughout the pathogenesis of renal IRI. In the injury phase, M1 macrophages contribute to inflammation and tissue injury, whereas M2 macrophages exert anti-inflammatory functions in post-ischaemic kidneys and facilitate renal tubular regeneration during the recovery phase. T cells also show dynamic changes in number and phenotype depending on the phase of renal IRI. CD4+ T cells have a substantial role in inducing renal tissue damage in the early injury phase. TREG cells increase in the late injury phase and facilitate tubular regeneration in the recovery phase. B cells are activated and differentiate in the injury phase, and limit tubular regeneration in the recovery phase. Abbreviations: DAMPs, damage-associated molecular patterns; IRI, ischaemia–reperfusion injury; NK, natural killer; TLR, Toll-like receptor; TREG cells, regulatory T cells.
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Figure 1: Major sexually transmitted disease pathogens detected in semen. |