Chapter 17: Specific Defenses Flashcards

1
Q

Specific (adaptive) defenses

A

-Adapt to invader and changes throughout life
-Specific recognition of antigen- lymphocytes (B and T) and antibodies
-Memory B and T cells and antibodies

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2
Q

Active naturally acquired immunity

A

Antigens enter the body naturally; body induces antibodies and specialized lymphocytes

Resulting from infection

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3
Q

Passive naturally acquired immunity

A

Antibodies pass to the fetus via placenta or to infant via breast milk

Transplancetal or via colostrum

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4
Q

Active artificially acquired immunity

A

antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes

Inj of Ag (vaccination)

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5
Q

Passive artificially acquired immunity

A

-performed antibodies in immune serum are introduced by injection
-Gamma globulins
-Antivenom

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6
Q

Humoral (antibody-mediated) immunity

A

B lymphocyte produce antibodies to extracellular antigens in body fluids (humors)

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7
Q

(Cellular) Cell-mediated immunity

A

-Specialized lymphocytes, mostly T cells, respond to intracellular antigens
-Intracellular Antigens include:
-Viruses, fungi, parasites, cancer
-Intracellular bacteria
-Chlamydia
-Rickettsia

-After maturing in the thymus, T cell migrate to lymphoid tissues
-By clonal selection T cells differentiate into activated (effector) T cells when stimulated by an antigen

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8
Q

Antigens (immunogens)

A

-Any substance that causes antibody formation
-Are usually proteins or large polysaccharides
-Often part (capsule, flagella- made up of protein) of the invading microbe exotoxin of the microbe
-Most have high molecular weight

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9
Q

Antigenic determinants

A

Antibodies recognize and react w/ Antigenic determinants or epitopes (region on antigen)

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10
Q

Haptens

A

-Molecules too small to stimulate antibody formation by itself
-Ex. penicillin- can cause allergic reaction, poison ivy
-Hapten molecules combine w/ Skin or plasma protein (carrier molecule) > hapten-carrier conjugate

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11
Q

Antibodies (immunoglobulins)

A

-Proteins made in response to the antigen (Ag, specific) and combines specifically to Ag
-In the Gamma Globulin fraction of serum
-Proteins will migrate base on charge and size
-Gamma (most (-)- cathode)
-Beta- neutral
-Alpha (most (+)- anode)
-Albumin more +
-Antibody binding site
-Hinge region- flexibility to accommodate epitope
-Fc (Stem) region
-Any cell that has Fc receptor can attach

-2 antigen binding sites (conine w/ epitopes on Ag) in V region of H and L chain
-Variable (V, specificity of antibody) and Constant (C, AA’s sequence os constant “stays the same, determines class of Ab)
-Fc region binds complement that has Fc receptor

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12
Q

Antibody structure

A

Polypeptide chains
-2 regions:
-V: variable region
-C: constant region- determine class

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13
Q

Antibody structure

A

A typical antibody monomer has 4 polypeptide chains
-2 identical light (L) chains
-2 identical heavy (H) chains

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14
Q

IgG antibodies

A

-G= gamma heavy chain
-Monomer
-80% of serum
-Fix complement
-Cross placenta neutralize toxins (exotoxins)
-Secondary immune response
-Second time antigen comes into host
-Gives lifelong immunity- why vaccines work
-Memory response
-Chronic infection

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15
Q

IgM antibodies

A

-M= Mu heavy chain
-Pentamer
-Includes J (joining) chain
-Fix complement- best
-Agglutinates microbes; appears first in infection (primary response)
-Best for agglutination
-What we make the first time we are exposed to infection- initial exposure/infection
-Does not cross placenta

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16
Q

IgA antibodies

A

-A= alpha heavy chain
-Dimer
-Includes J (joining) chain
-In secretions, blood, lymph
-Mucosal (along mucus membranes) protection

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17
Q

IgD antibodies

A

-D= delta Heavy chain
-Monomer
-In blood, lymph, on B cells
-B cell receptor
-On B cells, initiate immune response
-Does not cross placenta, cannot fix complement

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18
Q

IgE antibodies

A

-E= Epsilon Heavy chain
-Monomer
-On mast cells and basophils, in blood
-Allergic (type 1 immediate hypersensitivity (anaphylaxis)) reactions; lysis of parasitic protozoan worm
-Does not cross placenta- cannot fix complement

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19
Q

Components of lymphatic system

A

-Primary: bone marrow, thymus
-Secondary: lymph node, spleen, peyer’s patch (GALT), tonsils, adenoids

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20
Q

Differentiation of T cells and B cells

A

-Stem cell
-Diverges into 2 cells
-Develop in bone marrow or fetal liver
-Thymus
-differentiate to T cells in Thymus
-T cell
-TC receptor
-Cd molecules
-CD4, CDb
-Migrate to lymphoid tissue (spleen, lymph node)
-B cell
-IgD and IgM
-Red bone marrow
-Differentiate to B cells in adult red bone marrow

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21
Q

Clonal selection

A

1) stem cells differentiate into B cells, each bearing surface immunoglobulins against specific antigen
2) B cell 2 encounters its specific antigen and prolerates
3) Some B cells proliferate into long-lived memory B cells, which at a later date can be stimulated to become antibody-producing plasmocyte
4) other B cells proliferate into antibody-producing plasmocyte

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22
Q

Result of Ag-Ab binding: agglutination

A

-Reduces # of infectious units to be dealt w/
-Clumping

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23
Q

Results of Ag-Ab binding: opsonization

A

Coating antigen w/ antibody enhances phagocytosis

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24
Q

Results of Ag-Ab binding: complement fixation (activation)

A

-By classical pathways
-Causes inflammation (C3A and C5A) and cell lysis (C5-C9)

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Results of Ag-Ab binding: neutralization
-Blocks adhesion of bacteria and viruses to mucosa -Blocks attachment to toxin- antitoxin
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Results of Ag-Ab binding: antibody-dependent cell-mediated cytotoxicity
Antibodies attached to target cell cause destruction by macrophages, eosinophils and NK cells
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Antibody titer
-Is the amount of Ab in serum -Acute serum: within 1st wk -Primary response: 1st response to antigen- during acute infection -IgM low amount -Slow rise in antibody titer -1st IgM antibodies, followed by IgG -A gradual decline in titer occurs -Secondary response (memory) -Subsequent (second) exposure to antigen -When disease progresses- chronic infection -IgG -Stimulates rapid high IgG antibody titer -Mostly IgG produced for life long immunity
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Monoclonal antibodies
1) mouse is injected w/ a specific antigen that induce production of antibodies against that antigen 2) The spleen of the mouse is rem’d homogenized into cell suspension. The suspension includes B cells that produce antibodies against the injected antigen. 3) The spleen cells are then mixed w/ myeloma cells that are capable of continuous growth in culture but have lost the ability to produce antibodies. Some of the antibody-producing spleen cells and myeloma cells fuse to form hybrid cells. These hybrid cells are now capable of growing continuously in culture while producing antibodies. -Why do they want the spleen? -It is secondary lymphoid tissue 4) the mixture of cells is placed in a selective medium that allows only hybrid cells to grow 5) Hybrid cells proliferate (divide) into clones called hybridomas. Hybridomas are screened for production of the desired antibody 6) The selected hybridomas are cultured to produce large quantities of monoclonal antibodies. Isolated antibodies are used for treating and diagnosing disease. -The hybridoma cell culture is immortal and produces monoclonal Abs (Mabs) -Immunotoxins for cancer thera
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Interleukin-1
Stimulates Th cells (T-helper cells)
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Interleukin-2
Activates Th, B, Tc, and NK cells
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Interleukin-12
Differentiation of Cd4 T cell (T helper cells)
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Gamma interferon
Increase activity of macrophages (phagocytes)
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B cells
-Remain in bone marrow -Develop into a clone of plasma cells and memory cells -Responsible for humoral response -differentiates into antibody secreting plasmocytes and memory cells
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Cellular components of immunity
-Stem cells give rise to T cells -Mature T cells move to the Thymus
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Pathogens entering the GI or respiratory tract pass through…
M (microfold) cells in peyer’s patches (GALT- secondary lymphoid tissue) which contain dendritic cells which are antigen-presenting cells
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T cells
-Produce T cell receptors (TCRs) that recognize specific epitope on the antigen -Produce cluster of differentiation (CD) surface glycoproteins -Tc- cytotoxic T cell -Th- T helper cell -Mature in the thymus -Fight against intracellular pathogens -Recognize MHC antigen complexes on AC -develops from a stem cell processed in the thymus gland, that is responsible for cell-mediated immunity.
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Antigen presenting cells
-Dendritic cell -B cells -Macrophage
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Major Histocompatibility Complex (MHC)
-Consists of cell-surface proteins that are unique to each and provide Self and display molecules -On surface of Antigen presenting cells -T cells recognize antigens in association w/ MHC on the APC
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Major histocompatibility complex (MHC) classes
-MHC Class I are present on almost all nucleated cells; binds CD8 molecules -MHC Class II are present on special immune system cells; bind CD4 molecules
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Helper T cells (CD4, Th)
-bind to MHC II molecules -Th1- activate cells related to cell-mediated (T cells, macrophages) immunity via cytokines -Th2- activate B cells -Th17- stimulate the innate immunity
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Cytotoxic T cells
-bind to MHC I molecules -Cytotoxic lymphocytes (CTL): destroys target virus or cancer-infected cells on contact; generated from precursor T cytotoxic (Tc) cells -Tc are activated by endogenous (antigens inside the cell- target infected cells) antigens and MHC I on target cell -Precursor T cytotoxic cells (CTLp) are activated to become cytotoxic T lymphocytes (CTLs) -Activated into cytotoxic T lymphocyte w/ the help of Th cell via cytokines and costimulatory signals -CTLs release perforin (lysis) and granzymes that induce apoptosis (programmed cell death) in the target cell -Destroy virus-infected cells -CD8 (+) -Make a lesion in a target cell or induce apoptosis -Recognize antigens and MHC I complexes on APC
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T-regulatory cells (Tr)
-Formally suppressor T cells -Turn off immune response, maintains tolerance (unresponsiveness to self-antigens)
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Activation of T helper cells
-Antigen (Ag) is processed by APC -Antigen fragments associate w/ MHC II -Th cell are activated by Ag-MHC II complex on APCs -After binding an APC, Th cell or APC secretes a costimulatory molecule, activating the Th cell -Th cell secrete cytokines that cause it to become activated
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Activation of cytotoxic T cell
1) a normal cell will not trigger response by a Tc cell, but a virus infected cell or a cancer cell produces abnormal protein (endogenous antigens) that will trigger a response 2) Viral antigen fragments are present on the infected cell surface by classI MHC molecules 3) Tc cell is activated to produce a clone of cytotoxic T lymphocytes (CTLs) 4) The CTL induces the virus-infected cell to die by apoptosis
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How do macrophages become activated? (Nonspecific cells)
By cytokines or by ingesting antigen
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Nonspecific cells: NK cells
-Natural killer (NK) cells nonspecifically destroy virus-infected cells, tumor cells, and attack parasites -NOT a B Cell or T Cell- nonspecific -Includes granules -Lytic enzymes and apoptosis
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Antibody-dependent Cell-Mediated Cytotoxicity (ADDC)
-organism , such as many parasites, that are too large for ingestion by phagocytic cells must be attacked externally -By NK cells -Worms (helminths)
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Activation of B cells by T-independent antigens
-Repeating units cross-link several antigenic receptors on B cell -Directly stimulate/activate B cells -Doesn’t need help of T cell -Ex. capsule polysaccharide; lipopolysaccharide (only present in Gram-(-) bacteria)
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T-dependent antigens
-Stimulate formation of antibodies only w/ the assistance of a T helper cell -Are mainly proteins on viruses, bacteria, foreign RBC’s, and hapten w/ their carrier molecules
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Activation of B cells by T-dependent antigens
1) B cell receptor binds to antigen 2) antigen is endocytosed and fragmented 3) antigen fragment (peptides) are presented by MHC class II on the B cell 4) T cell binds MHC+ peptide present on the B cell; costimulatory molecules and cytokines activates the B cell 5) Clonal expansion of B cells results in antibody-secreting plasmocytes and memory B cells specific for the same antigen
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Duality of immune response: Humoral (antibody-mediated) immune system- control of freely circulating pathogens
1) B cell binds to the antigen for which it is specific. A T-dependent B cell requires cooperation w/ a Th cell 2) B cell, often w/ stimulation by cytokines from a Th cell, differentiates into a plasmacyte. Some B cells become memory cells -Cytokines from the Th cell transform B cells into antibody-producing plasmocytes 3) plasmocytes proliferate and produce antibodies against the antigen
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Duality of immune response: cellular (cell-mediated) immune system- control intracellular pathogens
1) T cell binds to MHC-antigen complexes on the surface of the infected cell, activating the T cell (w/ its cytokine receptors). -Cytokines activate Th cells -Cytokines from the Th cell transform B cells into antibody-producing plasmocytes -Cytokines activate macrophage 2) activation of macrophage (enhance phagocytic activity) 3) Tc cells become an activates cytotoxic T lymphocyte (CTL) able to induce apoptosis of the target cells
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T helper cell
-CD4 (+) -Recognize antigen and MHC II complexes on APC -Activates cells to make Ab -Activate cells relates to cell-mediated immunity
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Differentiate between non-specific and specific (adaptive) immunity.
Nonspecific (innate) immunity: -Broad response: Reacts to a wide range of pathogens in the same way. -Rapid response: Initiated quickly upon sensing a threat. -Examples: Skin, stomach acid, phagocytes (like macrophages and neutrophils), inflammation, and fever. -No memory: Doesn't develop memory for specific pathogens, so the response is the same each time. Specific (adaptive) immunity: -Targeted response: Recognizes and attacks specific antigens (foreign molecules). -Slower response: Takes longer to mount a defense compared to innate immunity. -Examples: T cells and B cells (lymphocytes) and their products (like antibodies). -Memory: Develops immunological memory after exposure to a pathogen, allowing for a faster and stronger response upon re-exposure.
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Compare and contrast the “two arms” of specific immunity which are cell mediated immunity (CMI) and antibody mediated immunity (AMI). AMI is also defined as humoral immunity.
Cell-mediated immunity: -Mechanism: T cells, specifically cytotoxic T cells (CTLs), recognize and destroy cells that are infected with pathogens or have become cancerous. -Role: CMI is crucial for fighting intracellular infections (like those caused by viruses and some bacteria) and eliminating tumor cells. -Key Players: T cells (including helper T cells and cytotoxic T cells). -Target: Infected cells. Antibody-mediated/humoral immunity: -Mechanism: B cells produce antibodies (also called immunoglobulins) that circulate in the body fluids and bind to antigens (specific molecules on pathogens or toxins). -Role: AMI defends against extracellular pathogens (like bacteria and viruses) and toxins by neutralizing them and marking them for destruction by other immune cells. -Key Players: B cells (which differentiate into plasma cells to produce antibodies). -Target: Free pathogens and toxins in body fluids.
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​Explain the function of antibodies and describe their structural and chemical characteristics. Diagram the clonal selection theory.
proteins produced by the immune system that bind to specific antigens, marking them for destruction or neutralizing their harmful effects. They have a Y-shaped structure consisting of two heavy and two light polypeptide chains. Clonal selection theory explains how the immune system generates a diverse antibody repertoire and how it selects the right cells to produce antibodies specific to a particular antigen. Structure: -Y-shaped structure: -Antibodies are composed of two heavy chains and two light chains, joined by disulfide bonds, forming a Y-shape. -Polypeptide chains: -The heavy chains (H chains) and light chains (L chains) are polypeptide chains that contribute to the overall structure and function of the antibody. -Antigen-binding sites: -The N-termini of the heavy and light chains form the variable regions, which create the antigen-binding sites (Fab regions). -Constant regions: -The remaining portions of the heavy and light chains (Fc regions) are constant and determine the antibody class and its effector functions.
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Explain five different ways that antibodies react with an antigen and identify the consequences of the reaction.
1. Neutralization: Antibodies bind to specific sites on antigens (like viruses or toxins) to block their ability to infect cells or cause harm. This prevents the antigen from interacting with its target, effectively rendering it harmless. 2. Agglutination: Antibodies bind to multiple antigens on the surface of a pathogen, like a bacterium, causing them to clump together. This makes it easier for phagocytic cells to engulf and destroy the pathogens, reducing their spread. 3. Opsonization: Antibodies coat antigens with a layer that increases their visibility and palatability to phagocytes. This enhanced recognition allows phagocytes, like macrophages and neutrophils, to more readily engulf and destroy the antigen-antibody complex. 4. Precipitation: When soluble antigens combine with antibodies, they form insoluble complexes that precipitate out of solution. This makes the antigen less soluble and more susceptible to phagocytosis. 5. Complement Activation: Antibodies bound to antigens can activate the complement system, a cascade of proteins that enhance immune responses. This activation can lead to several outcomes, including: -Lysis: Complement proteins can directly attack and lyse (burst) cells, like bacteria, destroying them. -Opsonization: Complement proteins can also act as opsonins, enhancing phagocytosis. -Inflammation: Complement activation can trigger inflammatory responses, attracting more immune cells to the site of infection.
58
Distinguish between a primary and a secondary immune response.
The primary immune response is the body's initial reaction to a foreign antigen, while the secondary immune response is the faster and stronger reaction to a subsequent exposure to the same antigen. The primary response takes longer to develop and involves the initial activation and differentiation of B and T cells, leading to the production of antibodies and immune memory. The secondary response, on the other hand, is mediated by memory cells formed during the primary response, resulting in a more rapid and effective immune response.
59
Compare and contrast T-dependent antigens and T-independent antigens.
T-dependent and T-independent antigens differ in their requirement for T cell help to stimulate antibody production by B cells. T-dependent antigens require T cell cooperation, while T-independent antigens can activate B cells without T cell assistance.
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Antigen
Any substance the causes antibody formation “immunogen”
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Antibody
A protein produced by the body in response to an antigen, and capable of combining specifically with that antigen
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Plasma cell
develop from B lymphocytes (B cells), a type of white blood cell that is made in the bone marrow. Normally, when bacteria or viruses enter the body, some of the B cells will change into plasma cells. The plasma cells make antibodies to fight bacteria and viruses, to stop infection and disease
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Monoclonal antibodies
Monoclonal antibodies (mAbs) are lab-produced proteins that mimic the body's own antibodies, acting as targeted therapies for various diseases, including some cancers. They are designed to recognize and bind to specific targets, such as proteins on the surface of cancer cells, and can be used alone or to deliver other therapies.
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Cytokines
A small protein released from human cells that regulates the immune response Directly or indirectly may induce fever, pain, or T cell proliferation
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Interferons
A specific group of cytokines Alpha and beta-INFs are antiviral proteins produced by certain animal cells in response to a viral infection. Gamma-INF stimulates macrophage activity.
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Interleukins
A chemical that causes T cell proliferation