CHAPTER 2 IMMUNO- Innate Immunity teil 2

They become phosphorylated on tyrosine residues.

They increase the permeability of blood vessels, allowing plasma proteins to enter tissues.

They break down microbial proteins.

They fuse with lysosomes, leading to their killing by enzymes and toxic substances.

Interferon-gamma (IFN-γ).

The collectin family.

The NK cells become activated and eliminate the virus-infected cells.

By binding to venular endothelial adhesion molecules in response to chemoattractants.

They are produced in phagolysosomes and kill microbes inside the cell.

Host cells infected by obligate intracellular microbes, such as viruses.

They deliver contents of their cytoplasmic granules into the infected cells.

Molecularly defined cytokines with specific numbers, e.g., interleukin-1.

Inhibition of cytokine and chemokine production and reduced expression of costimulators and class II MHC molecules.

They recruit blood neutrophils and monocytes to sites of infection.

It recognizes stress-induced molecules resembling class I MHC proteins.

A process where phagocyte oxidase converts molecular oxygen into superoxide anion and free radicals to kill ingested microbes.

They transition to a high-affinity state for their ligands.

They are activated by TLRs and other innate sensors as well as by cytokines.

Killer cell immunoglobulin-like receptors (KIRs) and receptors consisting of CD94 and NKG2.

In lysosomes and phagolysosomes.

NK cells and T cells.

Networks of chromatin extruded by dying neutrophils that trap and kill bacteria and fungi.

Chemokines, bacterial formyl peptides, and complement fragments C5a and C3a.

The flowing blood disrupts the binding; bonds reform downstream, allowing repetitive rolling.

IL-12, produced by macrophages, activates NK cells to secrete IFN-γ.

Interferon-γ (IFN-γ).

Opsonization and phagocytosis, inflammation, and cell lysis.

Phagolysosomes.

They are involved in tissue repair and terminating inflammation.

CD16, which recognizes the Fc region of bound IgG antibodies.

Activating NK cells, leading to increased killing activity and macrophage activation.

Redness, warmth, and swelling.

Inducible nitric oxide synthase (iNOS).

It binds to phosphorylcholine on microbes and opsonizes them for phagocytosis by macrophages.

The phagocytosis of complement-coated microbes and activation of macrophages.

The alternative pathway (microbe), classical pathway (microbe bound to antibody), and lectin pathway (microbe bound to mannose-binding lectin).

The NK cell is activated and kills the infected cell.

They are inflammation-inducing by-products released during complement activation.

Interferon-gamma (IFN-γ).

Transforming growth factor beta (TGF-β).

Phagocytes work with plasma proteins like complement to destroy offending agents.

Causes vasodilation and increased capillary permeability.

They activate leukocytes and stimulate their migration through the endothelium.

Leukocytes become oval in shape as they migrate.

The balance between activating and inhibitory receptors.

Ligands for integrins expressed by activated endothelial cells.

Type I IFNs.

Inhibition of inflammation and differentiation of regulatory T cells.

They migrate along extracellular matrix fibers directed by concentration gradients of chemoattractants.

Cytokines secreted by various immune cells.

They express somatically rearranged antigen receptors but have limited diversity.

γδ T cells, NK-T cells, mucosal-associated invariant T cells, B1 cells, and marginal zone B cells.

C3, a plasma protein.

The process of ingesting particles larger than 0.5 μm in diameter by phagocytes.

Lipid mediators (e.g., prostaglandins, leukotrienes) and cytokines (e.g., TNF).

M1 or pro-inflammatory macrophages.

Septic shock, characterized by low blood pressure.

In tissues.

They promote activation of cytosolic protein tyrosine phosphatases, counteracting ITAM functions.

By microbial products binding to TLRs and cytokines like NK cell-derived IFN-γ.

Dendritic cells, macrophages, mast cells, and ILCs.

Bone marrow.

In the skin, mucosal tissues, and most connective tissues.

Microbial products binding to TLRs, components of the complement system, or antibody-dependent mechanisms.

Histamine.

Through the sequential activation of proteolytic enzymes.

Activation of complement proteins on microbial surfaces where regulatory proteins are absent.

Antibodies that bind to microbes or other antigens.

Formation of a polymeric protein complex that causes osmotic lysis.

By sensing microbes and interacting with lymphocytes, especially T cells.

It protects them from destruction by NK cells.

ILCs may provide early defense against infections in tissues.

Injury leading to barrier break and microbe entry.

It promotes IFN-gamma production and increased cytotoxic activity in NK cells and T cells.

They are adhesion molecules that bind circulating neutrophils and monocytes to the endothelium.

Mannose-binding lectin (MBL) or ficolins binding to carbohydrate ligands on microbes.

Because it is initiated by a microbial product in the absence of antibody.

Response to pathogens and inflammatory mediators.

Most act on nearby cells (paracrine) or on the cells that produce them (autocrine).

IL-15, type I interferons, and IL-12.

The process of coating a microbe with molecules recognized by receptors on phagocytes, promoting binding and ingestion.

Tissue-resident cells that produce cytokines similar to helper T lymphocytes without expressing TCRs.

MBL recognizes microbial carbohydrates, coats microbes for phagocytosis, and activates the lectin pathway of complement.

Dendritic cells and macrophages.

Histamine, TNF, prostaglandins, and other mediators.

Macrophages, dendritic cells, mast cells, and other cells in tissues.

By blocking expression of class I MHC molecules in infected cells.

It is a protective response where circulating levels of plasma proteins increase rapidly after infection.

The NK cell is not activated and does not kill the normal cell.

Cytokines TNF and IL-1 acting on the endothelium of venules.

Viruses inhibit MHC expression, making it difficult for CTLs to recognize infected cells.

Selectin-mediated rolling, integrin-mediated firm adhesion, and chemokine-mediated motility.

Inherited deficiencies in integrins and selectin ligands leading to defective leukocyte recruitment and increased susceptibility to infections.

To eliminate infected cells and eradicate infections.

C3b covalently attaches to microbes and recruits downstream complement proteins.

Binding of membrane receptors to the microbe.

They provide defense against helminths and protect against snake and insect venoms.

Unaffected leukocytes prior to activation.

They initiate inflammation, stimulate adaptive immune responses, and capture and display protein antigens to T cells.

IFN-γ.

To engulf microbes and necrotic material and destroy potentially harmful substances.

Activation of cytosolic protein tyrosine kinases.

IFN-gamma.

They bind antibody-coated microbes and perform similar functions to complement receptors.

Macrophages, T cells, and mast cells.

An immunodeficiency disorder caused by inherited deficiency of the phagocyte oxidase enzyme.

They kill tumor cells as part of their immune response.

IFN-alpha: dendritic cells, macrophages; IFN-beta: fibroblasts, epithelial cells.

A collection of circulating and membrane-associated proteins important in defense against microbes.

Stimulates liver synthesis of acute-phase proteins and B cell proliferation.

They induce fever and stimulate liver cells to produce acute phase proteins.

The process by which NK cells kill antibody-coated cells.

Into three major groups based on their secreted cytokines corresponding to Th1, Th2, and Th17 subsets of CD4+ T cells.

High levels of bacterial PAMPs.

The acute inflammatory response, involving neutrophils and monocytes.

They increase the expression of endothelial adhesion molecules and chemokines to promote leukocyte movement.

C3b, which initiates the formation of the membrane attack complex (MAC).

Interleukin-1 (IL-1).

Increased integrin affinity, chemotaxis, and activation.

Ingesting and destroying microbes, clearing dead tissues, initiating tissue repair, and producing cytokines that regulate inflammation.

Tumor necrosis factor (TNF) and interleukin-1 (IL-1).

Integrins mediate firm adhesion of neutrophils to the endothelium.

Innate immune signals from TLRs and the cytokine IFN-γ.

Thrombus formation on endothelium and reduced blood pressure.

Phagocyte oxidase.

They crawl to and migrate through the junctions between endothelial cells.

Approximately 5% to 20%.

Injury to host tissues.

The interaction with selectins during weak tethering.

Pattern recognition receptors such as TLRs and NLRs, as well as phagocytic receptors like mannose receptors and scavenger receptors.

Classical (M1) and alternative (M2) pathways.

Interleukin-15 (IL-15).

They act as chemoattractants for leukocytes and activators of endothelial cells and mast cells.

Both the cell-mediated arm and the humoral arm of adaptive immunity.

By inhibiting viral replication and preventing the spread of infection.