Page 190 - Veterinary Immunology, 10th Edition

release from the bone marrow, their transendothelial migration,
VetBooks.ir and chemotaxis, thus increasing their accumulation within tissues.

Fever enhances their respiratory burst and accelerates caspase-
dependent neutrophil apoptosis. It also enhances the cytotoxic

activities of NK cells. With respect to adaptive immunity, raised
body temperatures cause dendritic cells to mature and enhance
multiple macrophage functions such as phagocytosis, release of NO
and cytokines, and expression of TLR2, TLR4, and MHC molecules.

Fevers enhance the passage of T cells across high endothelial
venules (Chapter 12), promote immunological synapse formation
(Chapter 14), and inhibit T cell apoptosis.

FIG. 7.2 The upregulation of both innate and adaptive immune
responses as a result of a fever.

High-mobility group box protein-1 (HMGB1) (Chapter 3) is a
potent sickness-inducing cytokine. Although IL-1, IL-6, and TNF-α
have long been known to cause septic shock and sickness behavior,
it is now clear that these three molecules induce slow release of

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