Ifn

Antiviral state

Virus

Antiviral state

Antibody -

Protection against infection

Neutralization

Virus

Neutralization

FIGURE 15-6 Innate and adaptive immune responses against viruses. A, Kinetics of innate and adaptive immune responses to a virus infection. B, Mechanisms by which innate and adaptive immunity prevent and eradicate virus infections. Innate immunity is mediated by type I interferons, which prevent infection, and NK cells, which eliminate infected cells. Adaptive immunity is mediated by antibodies and CTLs, which also block infection and kill infected cells, respectively.

FIGURE 15-6 Innate and adaptive immune responses against viruses. A, Kinetics of innate and adaptive immune responses to a virus infection. B, Mechanisms by which innate and adaptive immunity prevent and eradicate virus infections. Innate immunity is mediated by type I interferons, which prevent infection, and NK cells, which eliminate infected cells. Adaptive immunity is mediated by antibodies and CTLs, which also block infection and kill infected cells, respectively.

interferons by infected cells, especially dendritic cells of the plasmacytoid type (see Chapter 4). Several biochemical pathways trigger interferon production (Fig. 15-7). These include recognition of viral RNA and DNA by endosomal TLRs and activation of cytoplasmic RIG-like receptors by viral RNA. These pathways converge on the activation of protein kinases, which in turn activate the IRF transcription factors that stimulate interferon gene transcription. Type I interferons function to inhibit viral replication in both infected and uninfected cells by inducing an "antiviral state." The mechanisms by which interferons block viral replication were discussed in Chapter 4 (see Fig. 4-15).

NK cells kill cells infected with a variety of viruses and are an important mechanism of immunity against viruses early in the course of infection, before adaptive immune responses have developed. NK cells also recognize infected cells in which the virus has shut off class I MHC expression as an escape mechanism from CTLs because the absence of class I releases NK cells from a normal state of inhibition (see Fig. 4-6, Chapter 4).

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