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DPT 724 Pathophysiology > Lecture 3 Outline: Immunity Part 1 > Flashcards

Lecture 3 Outline: Immunity Part 1 Flashcards

1
Q

Innate Immunity

A
  • nonspecific and non-adaptive, natural immunity
  • first line of defense: skin and external body membranes
  • second line of defense: internal defenses (inflammatory response)
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2
Q

Acquired (Adaptive) Immunity

A
  • specific
  • overview (3rd line of defense)
  • has specific memory of antigens (adaptive)
  • results in specific responses to specific antigen (Ag)
  • result of active or passive processes
  • 2 components: humoral (B-cells) and cell-mediated (T-cells)
  • can be broken down into active and passive immunity as well
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3
Q

Active Immunity

A
  • protection acquired by introduction of an Ag into a responsive host which activates Ab’s or T-cells
  • expected to be permanent
  • vaccination is an example
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4
Q

Passive Immunity

A
  • Abs or sensitized lymphocytes transferred from one person to another
  • preformed Ab’s or T-cells are transferred from a donor to a recipient
  • transplacental or via breast milk from mother to child
  • does not result from formation of memory cells, only temporary immunity until antibodies are degraded
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5
Q

The Immune Response: Innate Immunity

A
  • exterior defenses: (1st line of defense) mechanical and chemical protection (ex: skin and mucosal membranes, lysozyme in tears, saliva, waxy secretions in ear canal, nasal hair, stomach acid, low pH vaginal secretions, acidic urine)
  • internal non-specific defenses (2nd line of defense)
  • internal can be inflammatory response, phagocytes, inflammatory mediators, natural killer cells, fever
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6
Q

Internal Non-Specific Defenses: Phagocytes

A
  • neutrophils (also called polymorphonuclear cells-PMN’s): fast, come right to scene, die after phagocytosis and often part of pus that drains
  • dendritic cells: best activators of immune system
  • monocytes: mature into macrophages once move from blood into tissue; macrophage phagocytosis is first step leading to a specific immune response; following phagocytosis expresses epitope of foreign Ag on surface which is recognized by helper T-cells–APCs, MHCII complex
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7
Q

Different Names for Helper T-Cells

A
  • helper/inducer lymphocyte
  • T4 lymphocyte
  • CD4 lymphocyte
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8
Q

Internal-Non Specific Defenses: Inflammatory Mediators

A
  • complement system
  • interferons: (IFNs, type of cytokine) diffuse into uninfected cells and bind to surfaces–stimulate macrophages and NK cells, stimulate production of antiviral proteins which block viral replication, suppress growth of tumor cells
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9
Q

Internal Non-Specific Defenses: Natural Killer Cells (NK)

A
  • large granular lymphocytes
  • await activation in thymus
  • recognize infected cells (d/t virus, bacteria or tumor) and directly attack and kill them (not by phagocytosis)
  • act before Ag specific immune system is activated
  • secrete potent chemical signals that enhance inflammatory response
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10
Q

Internal Non-Specific Defenses: Fever

A
  • pyrogens reset temperature set point in hypothalamus

- increases effects of antimicrobial substances produced by immune system (stimulates immune reactions)

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11
Q

The Immune Response: Acquired (Adaptive) Immunity

A
  • overview
  • acts to immobilize, neutralize, or destroy foreign substances and cells; acquired with exposure to foreign substances
  • amplifies inflammatory response and activates complement
  • is Ag-specific* system and has memory (*recognizes specific foreign molecules)
  • 2 types of responses to most pathogens: humoral or AMI (B-cells)-involved in producing Abs against epitopes, B-cell receptors bind free Ags or
  • Cellular or CMI (T-cells)-provide resistance through lysis of infected or abnormal cells, T-cell receptors bind processed Ag’s
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12
Q

Immunity Definition

A

-ability of body to defend itself against specific foreign invaders (molecules or cells)

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13
Q

Immunogenicity Definition

A

-ability to stimulate proliferation of specific lymphocytes and specific Ab production

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14
Q

Specificity Defintion

A

-Ag triggers focused immune defenses (from particular lymphocyte lineages) that respond only to Ag’s of this foreign substance/cell

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15
Q

Memory Definition

A

-immune system produces clones of specific memory lymphocytes (B and T) which react rapidly when the particular foreign substance/cell is encountered again

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16
Q

Antigens

A
  • any foreign substance that provokes specific immune responsess
  • antigenic determinants: parts of Ag’s that trigger specific immune response=Epitopes (small molecular group recognized by Ab’s, B and T cells)
  • epitopes protrude from surface, the more epitopes, the greater the antigenicity and the greater the immune response
  • ag receptor diversity: more than a billion different antigenic determinants are recognized by the body; need to be exact fit to trigger effects
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17
Q

Requirements for Antigenicity

A
  • foreignness (recognition of non-self)
  • large size
  • complexity
  • first two are most antigenic
18
Q

Major Histocompatibility Complex (MHC) Ag’s

A
  • proteins expressed on surface of all cells that allow self-recognition
  • unique to each individual’s cells: help in identifying self vs. foreign
  • 2 classes: Class I MHC and Class II MHC
19
Q

Class I MHC

A
  • found on all body cells except RBC’s

- recognized by T cells and APC

20
Q

Class II MHC

A
  • only on Ag presenting cells (APCs), thymus cells, and B-cells
  • synthesized in ER
  • phagosome containing pathogen (with exogenous Ag’s) merges with lysosome
  • MHC Class II proteins migrate into phagosome
  • Ag–MHC Class II complex migrates to cell membrane and displays antigenic peptide for recognition by CD4 helper T cells
21
Q

APC’s

A
  • phagocytose, process, and present Ag’s to lymphocytes
  • do not respond to specific Ags
  • actively migrate to lymph nodes and secondary lymphoid organs and present Ags to T and B cells
  • a T cell can only see anAg that has been processed (if not presented on cell surface it cannot be seen)
  • contribute to coordinating specific immunity: macrophages, dendritic (Langerhans) cells, B-cells
22
Q

Where are lymphocytes produced and developed?

A
  • mature and develop immunocompetence (ability to recognize specific Ag) in different locations
  • lymphoid organs: central and peripheral
  • central: thymus, bone marrow (B and T lymphocytes develop here)
  • peripheral: tonsils, lymph nodes, spleen
  • lymphocyte=small leukocyte found in lymph (ex: NK cells, T and B cells)
  • T cells mature in thymus and provide cell-mediated immunity
  • B cells mature in bone marrow and provide Ab mediated immunity
23
Q

Humoral Immunity (AMI)

A
  • antibody mediated immunity
  • circulating Ab’s present in humors of body (saliva, blood)
  • key player is B lymphocyte: surface receptor for specific Ag (membrane bound Ab’s), b-cells can only detect 1 Ag out of millions available
  • becomes activated when binding to Ag (along with helper T cell, which is needed to destroy the Ag): begins cloning itself into two types of B cells–memory B cells and plasma B cells which bind to Ag and tag it (opsonization) for phagocytosis (produces more Abs specific to that Ag)
  • Abs can activate complement system
  • more rapid than cell mediated response
  • can be transmitted to another person
  • B cells recognize Ag bound to surface –> B cells change into plasma cell/memory cell which makes Abs specific to that Ag
24
Q

Basic Ab Structure and Info

A
  • 4 polypeptide chains linked with disulfide bonds
  • 4 chains bound together form Ab monomer
  • each chain has a variable (V) region at one end and a constant region at other
  • variable regions of the heavy and light chains form Ag binding site (each B cell has different variable regions)
  • Abs are unique soluble proteins secreted by activated B cells and plasma cells in response to Ag
  • capable of binding specifically with that Ag
  • constitute much of the gamma globulin fraction of plasma proteins
  • also called immunoglobulins
25
Q

5 Classes of Ab’s (Immunoglobulins)

A
  • IgD: attached to surface of B cells, important in B cell activation
  • IgM: released by plasma cells during primary immune response
  • IgG: most abundant and diverse Ab in primary and secondary responses, crosses placenta and confers passive immunity
  • IgA: helps prevent attachment of pathogens to mucosal surfaces
  • IgE: binds to mast cells and basophils causing histamine release when activated
26
Q

Ab Mechanisms of Action

A
  • neutralization: Abs bind to and block specific sites on viruses or exotoxins thus preventing these Ags from binding to receptors on tissue cells
  • agglutination: Ab aggregation; cross-linking cells or particles into large clumps
  • opsonization: process of coating microorganisms or other particles with specific Abs (more readily recognized by phagocytes)
  • complement fixation: IgM and IgG Ab’s bound to cellular Ag’s bind complement via classical pathway (complement cascade causes chemotaxis, opsonization, phagocytosis and cell lysis; complement activation enhances inflammatory response)
27
Q

Ab Functions

A
  • all Abs form Ag-Ab complex
  • do not directly destroy Ag, though they may immobilize or inactivate Ag
  • act as opsonins and tag Ag for immune attack and destruction
  • defensive mechanism triggered by Abs include neutralization, agglutination, precipitation, opsonization, and complement fixation
28
Q

Cell-Mediated Immunity

A
  • T cell differentiation: CMI involved in most aspects of specific immune defense
  • different types of T-cells regulate specific immunity: helper T cells which carry CD4+ markers, suppressor T cells, memory T cells
  • following interaction with specific Ag, will produce additional lymphocytes: helper T cells or cytotoxic T cells
  • capable of turning the entire immune system on or off
  • cannot be transferred passively to another person
29
Q

Helper T Cells

A
  • 75% of all T cells
  • has T cell receptors on surface to bind to MHC II complex (dendritic cells best at activating it); activated by IL-1 from macrophages, when activated (non-naive) produce IL-2 interferon and other chemicals
  • these chemicals activate B cells to produce Abs
  • activate macrophages
  • help other T cells recognize and destroy virally infected cells
  • help NK cells kill infected cells
  • basic steps: 1. recognition by T cells of Ag presented by APC with matching MHC Class II markers 2. proliferation and differentiation of T cells once activated 3. production of clones of identical effector T cells capable of recognizing specific Ag 4. appropriate action (help, attack, memory, suppression) from T-cell subclones
30
Q

Cytotoxic T Cells

A
  • carry CD8+ markers destroy tumor cells and virus infected cells; also attack transplanted cells and tissues
  • attack infiltrated or abnormal cells (Abs of no use inside cell)
  • bind to MHC I complex and forces cell to kill itself
31
Q

How are the cells of the immune response different from cells of inflammatory response?

A
  • specificity
  • lasting “memory”
  • Ag induces an immune response
32
Q

T-Cell Activation Step 1

A

-Ag binding and Ag presentation

33
Q

T-Cell Activation Step 2: Co-Stimulation

A
  • T cells must bind to MHC Class II surface receptors on APC
  • after co-stimulation with cytokines, T-cells enlarge, proliferate and form clones
  • activated T-cells differentiate and perform functions according to T-cell class
34
Q

T-Cell Activity

A
  • primary T-cell response usually peaks within a week
  • T-cells then undergo apoptosis within a month
  • reduced activity parallels elimination of Ag
  • negative feedback control
  • few memory T-cells remain to respond to any future exposure to same Ag
35
Q

Helper T-Cells Pt 2

A
  • regulatory cells that play central management role in immune response
  • once primed by APC Ag presentation, helper T cells: stimulate proliferation of other T-cell classes, and stimulate B-cells that have already been bound to Ag
  • no coordinated immune response without helper T cell function
  • helper T cells interact directly with B cells that have Ag fragments on surfaces bound to MHC Class II receptors
  • helper T cells express CD4+ cell identify markers
  • helper T cells stimulate B cells to divide more rapidly and begin Ab formation
  • B cells may be active without helper T cell help by binding to T-cell-independent Ag’s
  • most Ag’s require helper T cell co-stimulation to activate B cells
  • cytokines released by helper T cells amplify nonspecific defenses
36
Q

Suppressor T Cells

A
  • immune regulatory cells which release cytokines that suppress activity of both T-cells and B-cells
  • generated with other specific T cell clones are generated
  • negative feedback control to bring the body back to normal after the battle has been won
37
Q

Cytotoxic T Cells Pt 2

A
  • express CD8+ identity markers
  • aka killer T cells are only T cells that can directly attack and kill other cells
  • circulate throughout body in search of body cells that display Ag to which they have been sensitized
  • targets include: virus-infected cells, cells with intracellular bacteria or parasites, cancer cells, foreign cells from blood transfusions or tissue and organ transplants
  • bind to self/anti-self complexes on any body cell
  • infected or abnormal cells can be destroyed as long as appropriate Ag and co-stimulatory regulators are present
  • in contrasts NK cells activate their killing machinery when they bind to a different MHC-related cell surface marker on cancer cells, virus-infected cells and transplant cells
38
Q

Cytotoxic T Lymphocyte Actions

A
  • secret perforins which cause cell lysis by creating transmembrane pores
  • secrete lymphotoxin which fragments the target cell’s DNA
  • secrete gamma interferon which stimulates macrophage attack
39
Q

Putting it All Together: Ab-Mediated Immunity

A
  • Ag challenge: first encounter between Ag and naive B cell
  • Ag presentation usually occurs in spleen or lymph node but can occur in any lymphoid tissue
  • Ag presentation usually made by macrophage, but some B-cells can react directly against certain bacterial Ag’s
  • binding of Ag to B cell specific Ag receptor activates B cell
40
Q

Putting it All Together: Primary Response

A
  • activated B cells grow and divide forming clones bearing same Ag-specific receptors and secreting same Ag-specific Ab
  • initial B cell differentiation, proliferation, and AB synthesis requires time after first Ag exposure
  • lag period 3-6 days after Ag challenge
  • peak plasma levels of Ab achieved in ~10 days
  • Ab molecules also reach interstitial fluids, especially where inflammation exists
  • Ab levels then decline gradually if there is no additional Ag exposure
41
Q

Putting it All Together: Secondary Response

A
  • Any subsequent exposure to same Ag
  • sensitized memory cells (B and T) respond within hours
  • Ab levels peak in 2-3 days at higher plasma levels than in primary response
  • activated B subclones generate Abs that bind with greater affinity
  • plasma Ab levels can remain high for weeks to months
42
Q

Putting it All Together: Immunological Memory

A
  • with any subsequent exposure, the immune system responds more quickly, forcefully
  • secondary response: Ab’s produced during subsequent exposures are produced in greater quantities and have greater attraction for Ag

DPT 724 Pathophysiology (18 decks)

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