immune Flashcards by Billy Vlobos

Inappropriate immune responses lead to

** allergies**

**autoimmune responses **

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The primary pathogens are

bacteria and viruses.

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are non-nucleated, single-celled micro-organisms

Bacteria

are non-nucleated, single-celled micro-organisms

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are not cellular, consisting of a nucleic acid enclosed by a protein coat

**
Viruses**

are not cellular, consisting of a nucleic acid enclosed by a protein coat

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Effector Cells

Never

Let

Monkeys

Eat

Banannas

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are highly mobile phagocytes

**Neutrophils **

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secrete chemicals that fight parasites

Eosinophils

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release histamine

Basophils

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change into macrophages (resident phagocytes)

Monocytes

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Lymphocytes are of two types

B lymphocytes
T lymphocytes

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lymphocytes

change into plasma cells that make antibodies

B lymphocytes

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Lymphocyte

are responsible for cell-mediated immunity

T lymphocytes

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A given leukocyte is present in the blood only ____________. Most are in the_______ on “defense missions”

A given leukocyte is present in the blood only _transiently. _ Most are in the tissue on “defense missions”

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Most leukocytes arise directly from

** stem cells in the bone marrow**

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Lymphocytes arise from lymphocyte colonies in

lymphoid tissue

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Two Intrinsic Defense Systems

Innate (nonspecific) system
Adaptive (specific) defense system

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Innate (nonspecific) system responds quickly and consists of:

First line of defense
Second line of defense

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– skin and mucosae prevent entry of microorganisms

First line of defense

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antimicrobial proteins, phagocytes, and other cells

Second line of defense

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Second line of defense – antimicrobial proteins, phagocytes, and other cells DO WHAT?

Inhibit spread of invaders throughout the body

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Second line of defense – its most important mechanism

Inflammation

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Adaptive (specific) defense system

THAT
– mounts attack against particular foreign substances

Third line of defense –

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Adaptive (specific) defense system

Takes longer to react than the innate system &
Works in conjunction with the innate system

Third line of defense –

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Adaptive (specific) defense system
Third line of defense – mounts attack against particular foreign substances
HUMORAL IMMUNITY CONTAINS-

B CELLS

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Adaptive (specific) defense system Third line of defense – mounts attack against particular foreign substances CELLULAR IMMUNITY CONTAINS

T-CELLS

Skin _________ (pH of 3 to 5) inhibits bacterial growth

Acidity

Skin \_\_\_\_\_\_\_\_\_\_\_contains chemicals toxic to bacteria

Sebum

\_\_\_\_\_\_\_in the skin: Presents a physical barrier to most microorganisms Is resistant to weak acids and bases, bacterial enzymes, and toxins

Keratin

Mucosae provide similar ________ barriers

mechanical

Mucosae provide similar mechanical barriers Stomach mucosae secrete concentrated\_\_\_\_\_\_\_ and protein-digesting enzymes

HCl

Mucosae provide similar mechanical barriers Saliva and lacrimal fluid contain \_\_\_\_\_\_\_\_

* * lysozyme * *

Mucosae provide similar mechanical barriers traps microorganisms that enter the digestive and respiratory systems

Mucus

Mucosae provide similar mechanical barriers Respiratory tract mucosae \_\_\_\_\_\_\_\_\_\_\_\_\_ in the nose trap inhaled particles Mucosa of the upper respiratory tract is \_\_\_\_\_\_\_\_\_ ______ sweep dust- and bacteria-laden mucus away from lower respiratory passages

1. **_Mucus-coated hairs_** in the nose trap inhaled particles 2. Mucosa of the upper respiratory tract is **_ciliated_** 3. **_Cilia_** sweep dust- and bacteria-laden mucus away from lower respiratory passages

The body uses nonspecific cellular and chemical devices to protect itself 1. 2. 3.

1. Phagocytes and natural killer (NK) cells 2. Antimicrobial proteins in blood and tissue fluid 3. Inflammatory response

derived from monocytes) are the chief phagocytic cells

Macrophages

wander throughout a region in search of cellular debris

Free macrophages

are fixed macrophages

Kupffer cells (liver) and microglia (brain)

become phagocytic when encountering infectious material

Neutrophils

are weakly phagocytic but important against parasitic worms

Eosinophils

- adherence more efficient if complement proteins or antibodies coat microbe

Opsonization -

Microbes adhere to the phagocyte by

“signature” carbohydrates

Phagocytosis Pseudopods engulf the particle into a

Phagosomes

Phagocytosis Phagosomes fuse with a lysosome to form a

phagolysosome

Phagocytosis Invaders in the phagolysosome are digested by

proteolytic enzymes

Phagocytosis Indigestible and residual material is removed by

exocytosis

Macrophages and other phagocytic cells have this & ## Footnote recognize specific classes of infecting microbes

Toll-like Receptors (TLRs)

Binding TLRs promotes phagocytosis and triggers the release of \_\_\_\_\_\_\_\_that promote inflammation

cytokines

React nonspecifically and eliminate cancerous and virus-infected cells

Natural Killer (NK) Cells

Natural Killer (NK) Cells Kill their target cells by releasing \_\_\_\_\_\_\_and other cytolytic chemicals \*Same method as Cytotoxic T lymphocytes

perforins

Natural Killer (NK) Cells Also secrete chemicals that enhance the

inflammatory response

The four cardinal signs of acute inflammation are

redness, heat, swelling, and pain

Inflammation Response Flood of inflammatory chemicals released into

extracellular fluid

Remember activated TLRs trigger the release of cytokines that promote inflammation Cytokine =

cell to cell signaling molecule

Inflammation Response WHAT IS released from basophils and mast cells in response to physical injury

Histamine

Inflammation Response WHAT IS released by injured tissue

Prostaglandins

Inflammation Response Cause local small blood vessels to dilate, resulting in

hyperemia

Inflammatory Response: Vascular Permeability Chemicals liberated by the inflammatory response ______ the permeability of local capillaries

increase

Inflammatory Response: Vascular Permeability —fluid containing proteins, clotting factors, and antibodies

Exudate—

\_\_\_\_\_\_\_\_\_\_\_seeps into tissue spaces causing local edema (swelling), which contributes to the sensation of pain

Exudate

The surge of protein-rich fluids into tissue spaces : 1. Helps dilute harmful substances 2. Brings in large quantities of oxygen and nutrients needed for repair 3. Allows entry of clotting proteins, which prevents the spread of bacteria

(edema):

Inflammatory Response: Phagocytic Mobilization Inflammatory chemicals diffusing from the inflamed site act as

chemotactic agents

Inflammatory Response: Phagocytic Mobilization 4 main phases

1. Leukocytosis 2. Margination 3. Diapedesis 4. Chemotaxis

– neutrophils are released from the bone marrow in response to leukocytosis-inducing factors released by injured cells

Leukocytosis

– neutrophils cling to the walls of capillaries in the injured area

Margination

– neutrophils squeeze through capillary walls and begin phagocytosis

Diapedesis

– inflammatory chemicals attract neutrophils to the injury site ## Footnote

Chemotaxis

Antimicrobial Proteins Enhance the innate defenses by:

1. Attacking microorganisms directly 2. Hindering microorganisms’ ability to reproduce

Antimicrobial Proteins The most important antimicrobial proteins are:

1. Interferon 2. Complement proteins

Genes that synthesize IFN are activated when a

host cell is invaded by a virus

Interferon molecules leave the infected cell and enter

neighboring cells

Interferon stimulates the neighboring cells to activate genes for an

antiviral protein

The antiviral protein nonspecifically blocks \_\_\_\_\_\_\_\_in the neighboring cell

viral reproduction

Complement System Can be activated in two ways

1. By exposure to molecules microorganisms surface 2. By exposure to antibodies (next lecture)

Complement System Does two things

1. Formation of Membrane Attack Complex that kills microbes 2. Augmentation of the inflammation

Complement can be activated by two pathways:

1. Classical pathway 2. Alternative pathway

Antibodies bind to invading organisms C1 binds to the antigen-antibody complexes (complement fixation)

Classical pathway

Triggered by factors B, D, and P, and polysaccharide molecules present on invading organisms

Alternative pathway

Both pathways(classical&alternative) converge on \_\_\_\_, which cleaves into C3a and C3b

\_\_\_\_\_\_ initiates formation of a membrane attack complex (MAC)

C3b

MAC causes cell ______ by allowing influx of water

lysis

C3b also causes\_\_\_\_\_\_\_\_\_, and C3a causes\_\_\_\_\_\_\_\_

opsonization and nflammation

The body’s thermostat is reset upwards in response to \_\_\_\_\_\_\_\_\_\_\_\_, ***_chemicals secreted by leukocytes and macrophages_*** exposed to bacteria and other foreign substances

** pyrogens **

High fevers are dangerous because they can

denature enzymes

Moderate fever can be beneficial, as it causes:

The liver and spleen to sequester iron (needed by microorganisms) An increase in the metabolic rate, which speeds up tissue repair

Why is Adaptive (Specific) Defenses a functional system?

1. Recognizes **_specific_** foreign substances - particular pathogens or foreign substances 2. Is _systemic - not restricted to initial infection site_ 3. Has _“memory” - after initial exposure, second response is stronger and faster_ 4. Also _amplifies inflammatory response_ and _activates complement_

adaptive(specific) immune system has two separate but overlapping arms called

1. Humeral, or antibody-mediated immunity 2. Cellular, or cell-mediated immunity

Antibodies freely circualte in the blood and lymph Bind bacteria, toxins, free viruses Marking for destruction is known as what immunity?

Humeral, or antibody-mediated immunity

What immunity is -Living cells protect against … Cells - infected with viruses, cancerous, from a graft

Cellular, or cell-mediated immunity

Compounds that elicit antibody production

Antibody generator

Antigens can be found on ?

surface of bacteria, on the surface of red blood cells, in pollens, in toxins, in food

Antigens can be an enormous variety of materials but what induces strong response

Proteins and polysaccharides

Y-shaped protein that has two regions:

Antibodies

Antibodies 2 region names

Fc Region Fab region

The constant region is the stem of the Y

Fc region

The two (identical) variable regions are the arms of the Y

(Fab region)

how can specific immunity be specific

variable region (Fab region) binds to a specific antigen

Two types of lymphocytes

B lymphocytes T lymphocytes

types of lymphocytes – oversee humoral immunity

B lymphocytes

type of lymphocytes – non-antibody-producing cells that constitute the cell-mediated arm of immunity

T lymphocytes

Play essential auxiliary roles in immunity

Antigen-presenting cells (APCs):

Antigen-presenting cells (APCs): what are the (professional APC)

1. Macrophage, 2. Neutrophil, 3. Dendritic cells

Lymphopoiesis involves

bone marrow thymus, peripheral lymphoid tissue

All lymphocytes begin maturation in

bone marrow

1. B cells finish maturation in the 2. T cells finish maturation in the 3. Mature but still “naïve” cells travel to

1. bone marrow 2. thymus 3. peripheral lymphoid tissue

first encounter between an antigen and a naive immunocompetent cell

Antigen challenge

Humoral Immunity Response Antigen challenge Takes place in the

spleen or other lymphoid organ

If the lymphocyte is a B cell: The challenging antigen provokes a \_\_\_\_\_\_\_\_ immune response \_\_\_\_\_\_\_\_\_\_\_ are produced against the challenger

If the lymphocyte is a B cell: The challenging antigen provokes a **_humoral_** immune response **_Antibodies_** are produced against the challenger

– cellular differentiation and proliferation, which occurs on the first exposure to a specific antigen 1. Lag period: 3 to 6 days after antigen challenge 2. Peak levels of plasma antibody are achieved in 10 days 3. Antibody levels then decline

Primary immune response

– **_re-exposure_** to the same antigen 1. Sensitized memory cells respond within **hours** 2. _Antibody levels peak in 2 to 3 days at much higher levels than in the primary response_ 3. _Antibodies bind with greater affinity_, and their _levels in the blood can remain high for weeks to months_

Secondary immune response

Active Humoral Immunity what encounters antigens and produce antibodies against them

B cells

response to a bacterial or viral infection

Naturally acquired –

response to a vaccine of dead or attenuated pathogens

Artificially acquired

spares us the symptoms of disease, and their weakened antigens provide antigenic determinants that are immunogenic and reactive

Vaccines –

Passive Humoral Immunity Differs from active immunity in the antibody source and the degree of protection by

1. B cells are not challenged by antigens 2. Immunological memory does not occur 3. Protection ends when antibodies naturally degrade in the body

Passive Humoral Immunity 1. – from the mother to her fetus via the placenta 2. – from the injection of serum, such as gamma globulin

1. **Naturally acquired** – from the mother to her fetus via the placenta 2. **Artificially acquired** – from the injection of serum, such as gamma globulin

Antibodies themselves do not destroy antigen; they

inactivate and tag it for destruction

All antibodies form an

antigen-antibody (immune) complex

Defensive mechanisms used by antibodies are: 1. 2. 3. 4.

Defensive mechanisms used by antibodies are: 1. **Complement fixation** 2. **Neutralization** 3. **Agglutination** 4. **Precipitation**

Main mechanism used against cellular antigens

Complement fixation

This triggers complement fixation and cell lysis

Antibodies bound to cells change shape and expose complement binding sites

Remember, complement activation also: 1. Enhances the\_\_\_\_\_\_\_\_\_\_response 2. Uses a \_\_\_\_\_\_ feedback cycle to promote phagocytosis 3. Enlists more and more \_\_\_\_\_\_\_\_ elements

Remember, complement activation also: 1. Enhances the **_inflammatory_** response 2. Uses a **_positive_** feedback cycle to promote phagocytosis 3. Enlists more and more **_defensive_** elements

– antibodies bind to and block specific sites on viruses or exotoxins, thus preventing these antigens from binding to receptors on tissue cells (mask dangerous parts of baterial exotoxins; viruses)

Neutralization

Cell bound antigens- - antibodies bind the same determinant on more than one antigen \*Makes antigen-antibody complexes that are cross-linked into large lattices

Agglutination

soluble molecules are cross-linked into large insoluble complexes

Precipitation

Antibody Structure consist of \_\_\_ polypeptide chains linked together with\_\_\_\_bonds Two identical heavy (H) chains and two identical light (L) chains

**_Four_** polypeptide chains linked together with **_disulfide_** bonds Two identical heavy (H) chains and two identical light (L) chains

Each chain of the Antibody has a \_\_\_\_\_ region at one end and a\_\_\_\_\_\_\_\_\_ region at the other

Each chain has a **_variable (V) region_** at one end and a **_constant (C)_** region at the other

What part of the Antibody structure combines to form the antigen-binding site

Variable regions of the heavy and light chains

To code for this many antibodies,\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_takes place: \*Gene segments are shuffled and combined in different ways by each B cell as it becomes \_\_\_\_\_\_\_\_\_\_\_\_ \*Random mixing of gene segments makes unique antibody genes that: Code for \_\_\_\_\_ of the H and L chain

To code for this many antibodies, **_somatic recombination_** takes place: Gene segments are shuffled and combined in different ways by each B cell as it becomes **_immunocompetent_** Random mixing of gene segments makes unique antibody genes that: Code for **_V region_** of the H and L chain

Antibodies responding to different antigens have ***_different_*** \_\_\_\_\_ regions but the \_\_\_\_\_ region is the ***_same for all antibodies_*** in a given class \_\_\_\_\_ regions form the stem of the Y-shaped antibody and **_determine the class of the antibody_**

** (V) Varible** **(C) Constant** **(C) Constant**

There are five classes of antibodies:

1. ** IgD** 2. **IgM** 3. **IgG** 4. **IgA,** 5. **IgE**

– monomer _attached to the surface of B cells*, important in B cell activation*_

**IgD**

– pentamer released by plasma cells during the primary immune response

** IgM** – _pentamer released by plasma cells_ during the _primary immune response_

– **_monome_**r that is the **_most abundant**_ and _**diverse_** _antibody in primary and secondary response_; crosses the _placenta_ and confers _passive immunity_

** IgG**

dimer that helps prevent attachment of pathogens to epithelial cell surfaces

** IgA** – dimer that helps **_prevent attachment_** of pathogens to epithelial cell surfaces

monomer that binds to _mast cells_ and _basophils_, causing histam**_ine_** release when activated

**_ IgE_** – monomer that binds to ***mast*** **_cells_** and _basophils_, causing histam**_ine_** release when activated

\_\_\_\_\_\_\_\_ are primarily **_helper_** T cells (TH) \_\_\_\_\_\_\_\_\_\_\_\_\_ are **_cytotoxic_** T cells (TC) that destroy cells harboring foreign antigens

**CD4 cells** (T4 cells) ** CD8 cells** (T8 cells)

\_\_\_\_\_\_\_\_\_\_ proteins – found on virtually all body cells \_\_\_\_\_\_\_\_\_ proteins – found on certain cells in the immune response

* *_Class I MHC_** proteins – found on virtually all body cells * *_Class II MHC_** proteins – found on certain cells in the immune response

* Found on almost all cells * **Always recognized by CD8 cytotoxic** T **cells** * _Display_ peptides from *_endogenous antigens_* *

Class I MHC proteins

* Found on B-cells and phagocytic cells * **_Always recognized by CD4 helper_** T cells * _Display peptides_ from **_exogenous antigens_**

Class II MHC proteins

They circulate throughout the body in search of body cells that display forign antigen on MHC I

TC cells, or killer T cells, cytoxic cells

The four major types of grafts are:

The four major types of grafts are: Autografts – Isografts – Allografts – Xenografts –

– graft _transplanted from one site on the body to another in the same person_

**_ Autografts_** – graft transplanted from one site on the body to another in the same person

– grafts between identical twins

**_ Isografts_** – grafts between identical twins

– transplants between individuals that are not identical twins, but belong to same species

Allografts – transplants between _individuals that are not identical twins, but belong to same species_

– grafts taken from another animal species

**_ Xenografts_** – grafts taken from _another_ animal _species_

Congenital and acquired conditions in which the *_function or production of immune cells, phagocytes, or complement is abnormal _*

Immunodeficiencies

Immunodeficiency- a genetic defect that producse: \***_A marked deficit in B and T cells_** Abnormalities in interleukin (chemokine that signals between WBCs) receptors or Defective adenosine deaminase (ADA) enzyme Metabolites lethal to T cells accumulate

SCID – severe combined immunodeficiency (SCID) syndromes

SCID is \_\_\_\_\_ if untreated; treatment is with\_\_\_\_\_

SCID is **_fatal_** if untreated; treatment is with **_bone marrow transplants_**

Acquired Immunodeficiencies – cancer of the lymph nodes leads to immunodeficiency by depressing lymph node cells

Hodgkin’s disease

– cripples the immune system by _interfering with the activity of helper T (CD4) cells_ Characterized by _severe weight loss, night sweats, and swollen lymph nodes Opportunistic infections occur, including pneumocystis pneumonia and Kaposi’s sarcoma_

Acquired immune deficiency syndrome (AIDS) –

\*Loss of the immune system’s ability to distinguish self from nonself \*The body produces autoantibodies and sensitized TC cells that destroy its own tissues

Autoimmune Diseases

Examples include multiple sclerosis, Type I (juvenile) diabetes mellitus, and rheumatoid arthritis

Autoimmune Diseases

Hypersensitivities categories: * Immediate * IgE-Mediated * E.g., anaphylactic shock *

* * Type I * *

Hypersensitivities categorie: * Cytotoxic * E.g., Blood transfusion reactions *

* * Type II * *

Hypersensitivities categorie: * Immune Complex (Ab/Ag)-Mediated * E.g., Disseminated intravascular coagulation in Gram-negative septicemia *

* * Type III * *

Hypersensitivities categorie: * Delayed Cell-Mediated * E.g., Tuberculin reaction

* * Type IV * *

* Caused by IgM and IgG (not IgE) * Onset is slow (1–3 hours) after antigen exposure * Duration is long lasting (10–15 hours)

Type II Hypersensitivities

* Antibodies bind to antigens on specific body cells, stimulating phagocytosis and complement-mediated lysis of the cellular antigens * Example: mismatched blood transfusion reaction

Cytotoxic (type II) reactions

\*Immune complexes are eliminated by phagocytosis \*with **excess of antigen** many small immune complexes are made “block” small capillaries (e.g., in kidney) Called **_Disseminated Intravascular Coagulation_**

Type III Hypersensitivities

Infection of blood (septicemia) by \_\_\_\_\_\_\_\_\_bacteria Leads to LPS in blood, immune complexes

Infection of blood (septicemia) by **_Gram-negative_** bacteria Leads to LPS in blood, immune complexes

Delayed hypersensitivities caused by cell-mediated immunity Poison ivy and poison oak Latex products Tuberculin skin test

Type IV Hypersensitivities