IgG and IgM—activate complement

IgG—opsonization

IgG and IgA—clear pathogens or neutralize toxins

Activated with the cooperation of macrophages, directly killing target cells

Secrete large amounts of IFN-y, promote macrophage activation, and promote Th1 cell differentiation

Recognize small phosphorylated molecules, proliferate and kill target cells

Secrete large amounts of IFN-y, promote macrophage activation, and promote Th1 cell differentiation

Neutrophils are the first to arrive at the site of infection and secrete defensins to destroy intracellular bacteria before they enter host cells.

After intracellular bacteria enter the host—phagocytic cells need to be highly activated and rely on IFN-y

If highly activated macrophages cannot clear the infection - granulomas form

Differentiate into Th1, release IFN-y to activate macrophages, and can activate CTL

Host cell MHC-I is downregulated, recognized by NK and initiated killing

Start ADCC

Secrete pro-inflammatory factors

Interferon

Begins to activate in the early stages of viral infection and generates a large amount of pro-inflammatory mediators

Free virus particles are taken up by APC and presented to Th cells via MHC-II.

Th1 cells provide IL-2 to CTL, and Th2 cells provide CD40L to B cells

Virus-specific CTL are key to antiviral immunity

Antiparasitic antibodies mediate neutralization, opsonophagocytosis, and activation of the classical complement pathway

→DC→NK/NKT activation

→NO production by macrophages →digestion and decomposition of protozoa

Upregulates digestive enzyme expression

Upregulate Fas expression

If the protozoa escapes from macrophage endosomes and enters the cytoplasm → MHC-I activates CTL

Secrete IFN-y to eliminate protozoa

Kill pathogens through cytotoxicity

Activation of B cells via CD40L-CD40

Induction and secretion of IgE via IL-4

Production of SIgA