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PA Immunology
Vanders Ch 18
Question | Answer |
---|---|
Site of production for Neutrophils | Bone marrow |
Site of production for Basophils | Bone marrow |
Site of production for Eosinophils | Bone marrow |
Site of production for Monocytes | Bone marrow |
Site of production for Lymphocytes | Mature in bone marrow (B cells and NK cells)and thymus (T cells); activated in peripheral lympoid organs |
Site of production for Plasma cells | Peripheral lymphoid organs; differentiate from B cells during immune responses |
Site of production for Macrophages | Bone marrow; reside in almost all tissue and organs; differentiate from monocytes |
Site of production for Dendritic cells | Almost all tissues and organs; microglia in the CNS |
Site of production for Mast cells | Bone marrow; reside in almost all tissues and organs; differentiate from bone marrow cells |
Functions of Neutrophils | Phagocytosis; Release chemicals involved in inflammation (vasodilators, chemotaxins, etc) |
Functions of Basophils | Carry out functions in blood similar to those of mast cells in tissues |
Functions of Eosinophils | Destroy multicellular parasites; Participate in immediate hypersensitivity reactions |
Functions of Monocytes | Carry out functions in blood similiar to those of macrophages in tissue |
Functions of Lymphocytes | Serve as recognition cells in specific immune responses and are essential for all aspects of these reponses |
Functions of B cells | Type of Lymphocyte; Initiate AB-mediated immune responses by binding specific antigens to the B cell's plasma membrane receptors; transformed into plasma cells during activation and secrete AB's; Present antigen to helper T-cells |
Functions of Cytotoxic T cells (CD8 Cells) | Bind to antigens on plasma membrane or target cells (virus-infected cells, cancer cells, and tissue transplants) and directly destroy the cells |
Functions of Helper T cells (CD4 Cells) | Secrete cytokines that help to activate B cells, cytotoxic T cells, NK cells, and macrophages |
Another name for Cytotoxic T cells are... | CD8 cells |
Another name for Helper T cells are... | CD4 cells |
Functions of NK cells | Bind directly and nonspecifically to virus-infected cells and cancer cells to kill them; Function as killer cells in antibody-dependent cellular cytotoxicity (ADCC) |
ADCC stands for... | antibody-dependent cellular cytotoxicity |
Functions of Plasma cells | Secrete antibodies |
Functions of Macrophages | Phagocytosis; Extracellular killing via secretion of toxic chemical; Process & present antigens to helper T-cells; Secrete cytokines involved in inflammation, activation and differentiation of helper T-cells, and systemic responses to infection or injury |
Functions of Dendritic cells | Phagocytosis; Extracellular killing via secretion of toxic chemical; Process & present antigens to helper T-cells; Secrete cytokines involved in inflammation, activation and differentiation of helper T-cells, and systemic responses to infection or injury |
Functions of Mast cells | Release histamine and other chemicals involved in inflammation |
Source of IL1 | Antigen-presenting cells such as macrophages |
Source of TNF | Tumor Necrosis Factor; Antigen-presenting cells such as macrophages |
Source of IL6 | Antigen-presenting cells such as macrophages |
Source of IL2 | Most immune cells |
Source of Interferons | Most cell types |
Source of Interferon-gamma | NK cells and activated helper T cells |
Source of Chemokines | Damaged cells, including endothelial cells |
Source of Colony-stimulating factors | Macrophages |
Target cells of IL1, TNF, and IL6 | Helper T cells; certain brain cells; numerous systemic cells |
Target cells of IL2 | Helper T cells; cytotoxic T cells; NK cells; B cells |
Target cells of Interferons | Most cell types |
Target cells of Interferon-gamma | NK cells and macrophages |
Target cells of Chemokines | Neutrophils and other leukocytes |
Target cells of Colony-stimulating factors | Bone marrow |
Major functions of IL1, TNF, and IL6 | Stimulate IL2 secrettion and IL2 receptor expression; induce fever; stimulate systemic responses to inflammation, infection, and injury |
Major functions of IL2 | Stimulate proliferation; Promote conversion to plasma cells |
Major functions of Interferons | Stimulate cells to produce antiviral proteins (nonspecific response) |
Major functions of Interferon-gamma | Stimulate proliferation and secretion of cytotoxic compounds |
Major functions of Chemokines | Facilitate accumulation of leukocytes at sites of injury and inflammation |
Major functions of Colony-stimulating factors | Stimulate proliferation of neutrophils and monocytes |
Source of Complement | Generated from enzymatic action on plasma proteins |
Source of Histamine | Secreted by mast cells and injured cells |
Source of Eicosanoids | Secreted by many cell types |
Source of Cytokines, including chemokines | Secreted by injured cells, monocytes, macrophages, neutrophils, lymphocytes, and several nonimmune cell types, including endothelial cells and fibroblasts |
Exaggerated specific responses to non-pathogenic environmental antigens are... | allergies |
Any exaggerated specific responses that are tissue damaging | hypersensitivities |
Specific, exaggerated and destructive responses to self antigens | auto-immunities |
Variable responses to self, neoantigens | cancers |
Strong barriers to organ and tissue transplantation | allogeneic responses |
How are acute inflammation chemical mediators produced? | Chemical mediators are produced (a) by phagocytic macrophage resident in the inflamed site, (b) by damaged cells in the tissue and (c) through activation of serum complement proteins |
Chemical mediators of acute inflammation include.. | histamine, serotonin, prostaglandins, leukotrienes, kinins, chemokines, cytokines, and anaphylatoxins |
Mediators of Early Acute inflammation will | attract WBC to the inflamed site and activation; effects rapid and affect the epithelial cells of neighboring blood vessels, leading to inc. blood flow, inc. fluid permeability and adhesiveness for circulating WBCs; accumulation of neutrophils |
the body’s defense mechanism in response to tissue damage and/or infection is | Inflammation |
The purpose of inflammation is to... | identify the area affected and call into play mechanisms that lead to elimination of the inflammatory stimulus and healing |
What are the most common initiators of inflammation? | Infection, trauma (physical or chemical), and pathologic immune responses |
Innate, non-specific defenses include | Physical and/or chemical barriers (epithelia); Molecular--complement, cytokines, chemokines, acute phase proteins (collectins);Cellular-phagocytic cells, natural killer (NK) cells |
Acquired, adaptive, specific defenses include | Molecular- antibodies;Cellular- lymphocytes: naive, effector, and memory lymphocytes |
The Responses by Both Defense Systems (Innate and Acquired) to Infection Consist of Two Phases: | Recognition of a potential pathogen and/or its products by host cells and molecules; Recruitment and/or generation of destructive effector mechanisms to contain or eliminate the potential pathogen and/or its products |
Which two cells play a role in activating the adaptive immune system and act as antigen presenting cells for T lymphocytes | macrophage and dendritic cells |
What is the origin of cells involved in defense? | Hematopoietic stem cell |
50-70 percent of all blood leukocytes are... | Neutrophils (the classic phagocytic cell), constantly replenished from bone marrow |
The precursors to all tissue macrophage; 1-6 percent of all blood leukocytes | Monocytes |
the tissue-specific, fully differentiated, highly phagocytic descendents of blood monocytes | Macrophages |
When partly activated, these cells can also be antigen-processing and presenting cells | Macrophages |
Antigen processing and presenting cells; <<1 percent of all blood leukocytes | Dendritic cells |
What 2 cells are sentinel cells detecting danger signals and initiating inflammation and may also serve as antigen processing and presenting cells and activate T lymphocytes? | Dendritic cells and macrophage cells |
Which type of cells detect virally infected host cells and may lead to cytolysis of the infected cells thus limiting the focus of infection? | NK cells |
Describe PRR's | Pattern Recognition Receptors; Direct uptake of pathogens by phagocytes and dendritic cells; (macrophage mannose receptorsor scavenger receptors); Triggering signaling pathways (ex. TLR) to produce anti-microbial peptides and inflammatory cytokines |
TLR stands for... | Toll-like receptors; once activated, it is a signaling pathway that produces anti-microbial peptides and inflammatory cytokines |
Explain the difference between inflammatory cytokines and chemokines | Inflammatory cytokines--molecules that affect the biological activity of other cells having specific receptors for these cytokines;Chemokines--molecules that attract other cell types along a chemical gradient |
How many families of chemokines are there? | 2 families: One family attracts monocytes, effector T lymphocytes and memory T lymphocytes; The other family attracts neutrophils and naïve T cells |
Function of IL-1 | Activates vascular endothelium and induces acute phase protein production and lymphocyte differentiation; local effect |
Function of IL-6 | Induces acute phase protein production and lymphocyte differentiation; systemic effect |
Function of IL-8 | Chemokine attracting leukocytes to the inflamed site, activates neutrophils; local effect |
Function of IL-12 | Activates NK cells and induces CD4+ TH1 lymphocytes; local effects |
Function of TNF alpha | Activates vascular endothelium, increase vascular permeability and induces acute phase protein production; local effect |
Autocrine vs paracrine in relation to cytokines | Autocrine: having an effect on the cell that produces the cytokine. The cell has receptors for the cytokine it produces; Paracrine: having an effect on cells in the near vicinity that have receptors for the cytokine |
Systemic Effects of the Inflammatory Cytokines IL-1, IL-6 and TNFa on the liver | Systemic effects: Stimulate the production of acute phase proteins CRP and mannose binding protein (MBP);Consequences: Complement activation, opsonization, phagocytosis |
Systemic Effects of the Inflammatory Cytokines IL-1, IL-6 and TNFa on bone marrow | Systemic effects: Stimulate the production of leukocytes; Consequences: Increased numbers of phagocytes, in particular, neutrophils |
Systemic Effects of the Inflammatory Cytokines IL-1, IL-6 and TNFa on the hypothalamus | Systemic effects: Induce fever indirectly by stimulating the hypothalamus; Consequences: Elevated temperatures inhibit viral and bacterial growth and increase antigen presentation |
Systemic Effects of the Inflammatory Cytokines IL-1, IL-6 and TNFa on fat and muscles | Systemic effects: Increase metabolism, contributing to the increase in body temperature; Consequences: Elevated temperatures inhibit viral and bacterial growth and increase antigen presentation |
Sepsis results in... | generalized production of very large amounts of TNFa by macrophage in the spleen and liver and the secretion of high concentrations into blood with resulting vascular collapse and shock |
Localized production of TNFa by tissue macrophage leads to... | inflammation and mobilization of cells to the site of infection |
What are Acute phase proteins? Give examples of them | Acute phase proteins are synthesized by the liver in response to macrophage cytokines. Ex. CRP and mannose-binding protein |
What is CRP? | An acute phase protein; C-Reactive Protein (CRP) is specific for microbial phosphorylcholine, is an opsonin, and can also activate serum complement |
What is MBP? | Acute phase protein; Mannose binding protein (MBP) recognizes mannose uniquely expressed by microbes;MBP is an opsonin, leading to enhanced phagocytosis;MBP also activates serum complement |
What are three interdependent pathways for initiating the activation of complement? | The lectin pathway initiated by MBP; The alternative pathway promoted/protected by microbial surfaces;The classical pathway initiated by antibody |
What is the central and most important serum complement component of all pathways | C3 |
Activation of the Alternative Pathway without Antibody | Naturally occurring proteases can cleave small amount of C3 in solution.This activated C3 can bind a 2nd component B, activated by an enzyme D to form a very labile C3 convertase that can cleave more C3b |