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Advanced Patho Test 1 > TEST 2: Immunity > Flashcards

TEST 2: Immunity Flashcards

1
Q

$ Innate Immunity (nonspecific response)

A

-The body’s first line of defense against pathogens (present from birth)
-Provides immediate, non specific protections against variety of pathogens
-physical barrier: skin, mucous membranes, stomach acid
-Cell components: phagocytes, Natural killer cells, dendritic cells
-Triggers rapid inflammation to combat infections and initiate immune response
-Role: Provides immediate protection against pathogens while adaptive immune response is developing
-recognizes common patterns on pathogens and triggers response

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2
Q

$ Adaptive Immunity (acquired)

A

-Occurs after innate immunity has been activated
-Is specific and acquired response that develops throughout life following exposure to pathogens
-Is highly specific and targets specific antigens on pathogens (based on immunologic memory, so upon reinfection there’s a stronger faster response)
-Involves two main branches:
1. Cellular mediated by T lymphocytes
2. Humoral mediated involving B lymphocytes and antibodies
-Have receptors that specifically recognize and respond to antigens

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3
Q

Antibody response in Innate Vs. Adaptive Immunity

A

-Innate: does not involve specific antibodies. Instead, it relies on protein mediators (complement proteins and cytokines)
-Adaptive: involves production of specific antibodies (immunoglobulins) by B cells

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4
Q

$ Antigen
(ANYTHING foreign to your body)

A

-The invader
-A molecule that can trigger an immune response
-Can be foreign substances like bacteria, viruses, allergens, fungi, or self-antigens in autoimmune conditions
-Role in adaptive immunity: are essential for initiating adaptive immune response, immune system recognizes antigens as foreign invaders and mounts targeted response to combat/ eliminate them

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5
Q

$ Haptens

A

-Too small of a molecule to be immunogenic but can elicit an immune response only when attached to a larger carrier protein molecule
-ie poison ivy or allergy to PCN

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6
Q

$ Antibody
Aka “Immunoglobulin”

A

-Glycoproteins produced by B lymphocytes in response to the presence of antigens
-Classified as IgG, IgM, IgE, IgA, IgD

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7
Q

$ Short term immunoglobulin
(IgM)

A

-first immunoglobulin produced in response to an infection
-Efficient at neutralizing pathogens and activating the complement system
-IgA (mucosal immunity) and IgE (allergic responses) are also considered short term antibodies

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8
Q

$ Long term immunoglobulin
(IgG)

A

-The main antibody class responsible for long term immunity
-Provides lasting protection against pathogens and enhances immune memory

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9
Q

$ Antigen Presenting Cell
(APC)

A

-Are specialized immune cells that detect, phagocytize, and present antigenic peptides to T lymphocytes to initiate adaptive immune responses
-Play a crucial role in activating T cells (key plays in adaptive immune response)
-By presenting antigens to T cells l, they ensure that the adaptive immune system can target and eliminate pathogens
-Examples: dendritic cells, macrophages, B cells

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10
Q

Structure of Immunoglobulins
Aka antibodies

A

-Have a characteristic Y shaped structure, consisting of 2 identical heavy chains and 2 identical light chains linked by disulfide bonds
-The Y shaped molecule has 2 antigen binding sites located at the tips of the arms, allowing antibodies to recognize and bind to specific antigens with high affinity

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11
Q

Immunoglobulin A (IgA)

A

-Found mainly on mucosal areas like resp/ GI tract
-Crucial role in mucosal immunity and defense

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12
Q

Immunoglobulin M (IgM)

A

-FIRST antibody produced in response to infection
-Involved in primary immune response and acts as potent activator of complement system

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13
Q

Immunoglobulin G (IgG)

A

-Most abundant antibody in bloodstream
-Provides long term immunity
-Can cross the placenta
-Key role in immune memory

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14
Q

Immunoglobulin E (IgE)

A

-Primarily involved in allergies responses and defense against parasitic infections
-Binds to mast cells and basophils, triggering the release of histamine in response to allergens

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15
Q

Immunoglobulin D (IgD)

A

-Found mainly on the surface of B cells, where to functions as a receptor for antigen recognition
-Involved in B cell activation and maturation

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16
Q

$ Generic T vs. B cells

A

T Cells: CELLULAR IMMUNITY
-Primarily target intracellular pathogens and abnormal cells
-Stimulate cytokines to activate leukocytes response or kill target directly
-Don’t produce antibodies
-slower to respond
-when impaired, more likely to have opportunistic infection

B Cells: HUMORAL IMMUNITY
-Combat extra cellular pathogens by producing antibodies
-Secrete antibodies to fight antigens
-Respond quickly on recognition of antigen
-When impaired, systemic responses to infection and more susceptible to encapsulated organisms

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17
Q

$ T Cells

A

-Maturation: Mature in the thymus gland
-Immunity: key layers in cell mediated immunity, responding to intracellular pathogens and abnormal cells
-Antigen response: Recognize and kill antigens by antigen presenting cells and respond directly by killing infected (cytotoxic T cells) or coordinating immune responses (helper T cells)
-Mature Cell Result: mature T cells give rise to various subtypes with specific roles in immunity
-Impairment consequences: can lead to compromised cell mediated immunity, making people more susceptible intracellular pathogens and cancer.

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18
Q

$ B Cells

A

-Maturation: mature in the bone marrow
-Immunity: produce antibodies that target extracellular pathogens
-Antigen response: recognize antigens directly and differentiate into plasma cells that produce antibodies targeting the specific antigen
-Mature cell Result: differentiate into plasma cells that produce antibodies to neutralize pathogens and memory B cells for future immune responses
-Impairment consequences: can result in decreased antibody production, reduced ability to fight off extracellular pathogens and increased susceptibility to infection

19
Q

Lymphocytes in waiting

A

-T cells produced in thymus
-B cells provides in bone marrow
-Move to secondary lymphoid cells (waiting rooms) ie lymph nodes, spleen,
Tonsils, adenoids
-Macrophages role if there’s a known antigen
-Dendritic cells role if unknown antigen

20
Q

$ T cell maturation

A

-Occurs in the thymus
-2 chains join to make 1 specific antigen receptor
-3 categories of T cells:
1. Helper
2. Regulatory
3. Cytotoxic

When they mature, differentiate into:
1. Memory T cells (CD2) located on cell surface and work as marker for T cells
2. Helper T cells (CD4) help activate CD8, NK, and B cells
3. Regulator T cells (CD4) help prevent autoimmune response
4. Cytotoxic T cells (CD8) binds to surface antigens and destroy infected cells

21
Q

$ B cell maturation

A

-Occurs in the bone marrow
-Have antigen binding sites
- 2 roles:
1. Once activated, produces daughter cells that make plasma cells (these cells
Are the antibody factories) and secrete IgM directly to the antigen
2. Turn into memory cells

22
Q

$ B cell response

A

-Primary: initial exposure
-IgM production (7 days after exposure)
-IgG production (is most of the antibodies accounted for)
-Levels gradually decrease

-Secondary response (subsequent exposure)
-IgG produced quickly in large amount and levels remain elevated

-Examples: vaccines with boosters, drug allergies

23
Q

$ Antibodies overview

A

-Circulate and protect from infection
-Antibodies protect by:
1. Neutralization: can inactivate antigens by binding to and neutralizing harmful components (preventing interaction with the host cell); block the antigens ability to cause harm
2. Opsonization (flagging of the antigen): can opsonize antigens by binding to their surfaces, making them more recognizable to macrophages and neutrophils (enhances the process of phagocytosis)
3. Agglutination: can cause this by cross linking multiple antigens (leading to the formation of antigen-antibody complexes); they help aggregate antigens which makes it easier for phagocytic cells to engulf them
4. Precipitation: can promote this by making soluble antigens insoluble, cause them to form complexes that precipitate out of solution (this leads to their aggregations and deposition, facilitating their removal by phagocytes)

24
Q

$ 4 ways antibodies provide protections from antigens overview

A
  1. Neutralization: prevents antigens from exerting harmful effects
  2. Opsonization: enhances phagocytosis of antigens by immune cells
  3. Agglutination: facilitates removal of antigens by clustering them together
  4. Precipitation: aids in the clearance of insoluble antigens from the body
25
Q

Direct effects antibodies have on antigens

A

-Bind to antigens to block their receptor sites preventing them from attaching to host cells and causing infection (ie vaccination)
-Have the ability to neutralize toxins and suppress their harmful effects (prevent toxins from getting into host cells and causing damage) ie tetanus

26
Q

$ Indirect effect antibodies have on antigens

A

-Activation of the innate immune response
-IgM: activate the complement system
-IgA: Opsonization

27
Q

$ Two types of adaptive immunity

A
  1. Acquired (active)
  2. Passive
28
Q

Acquired (active) immunity

A

-Is a specific and long lasting immune response that is developed after exposure to antigen or immunization
-Highly specific to particular pathogens or antigens
-Development of immunological memory (robust responses)

-Two arms of it:
1. Cellular immunity: T lymphocytes directly attack infected/ abnormal cells and coordinate immune response
2. Humoral immunity: B lymphocytes produce antibodies to target pathogens, neutralize toxins, tag particles to kill
-Primary response: lag time
-Secondary response: quickly recognize and mount a response
-Examples: chickenpox, measles, Covid

29
Q

$ Passive immunity (acquired)

A

-You yourself did nothing to acquire
-Transferred from mother to baby (natural passive) or introduction antibodies from someone else (artificial passive)
-Example: maternal antibodies, rabies antibodies for those exposed to

30
Q

$ Acquired (active) immunity vs. passive immunity (both are adaptive)

A

ACQUIRED: INTERNAL SOURCE
-Produced after an exposure to antigen/ immunization
-Requires host immune system response
-Generates long term memory
-Ex. Chickenpox, measles, Covid

PASSIVE: EXTERNAL SOURCE
-Antibodies and T lymphocyte are transferred from donor to recipient
-No host immune response
-Immediate protection but temporary
-Ex. Maternal antibodies, rabies antibody

31
Q

$ Key time periods for fetal/ newborn immunity

A
  1. Maternal antibodies: passive immunity provided by the mom protects baby until 37-40 weeks gestation (levels decrease after birth but can last about 6 months in babies systems)
  2. T and B cell production: begins are 6-8 months after birth (significant milestone in building babies immunity)
  3. Weak leukocytes at birth: are weak and less lethal at birth, making newborns more susceptible to infection until immune system strengthens over time
  4. Breast milk and immunoglobulins: breast milk contains various immunoglobulins that give passive immunity to baby and protect against infections (additional layer of defense as immune system is developing).
32
Q

Major Histocompatibility complex

A

-ALL cells (except RBC’s) have glycoprotein markers on the surface
(inherit one from each parent)
-HLA type: combinations of MHC markers play a role in human leukocyte antigen (6 basic types, trillions overall)
-these identify cells as self
-When one of these antigen isn’t present, someone may develop antibodies to it on exposure= graft/ transplant rejection
-Has a secondary role in controlling the quality and quantity of immune response

33
Q

Secretory immune response In mucosal system (acquired adaptive response)

A

-Systemic immune response in mucosal system: Lacrimal, salivary, bronchial,
Breast, GI/GU glands
-Plasma cells in secretory organs produce antibodies in secretions
-These antibodies are secreted and act locally (IgA= breastfeeding passive immunity)

34
Q

$ Age related immune transitions

A
  1. T cells: less likely to make more, leading to a weakened adaptive response
  2. B cells: number remains stable, but less responsive to new antigens, leading to a reduced ability to mount robust immune responses
  3. Chronic inflammation: tendency for immune system to be chronically activated leading to increased inflammation (aka “inflammaging”) sustained response can contribute to disease development
  4. Effect on chronic illness: changes in b/t cell function coupled with chronic inflammation can have detrimental impact on progression of chronic diseases. Weakened immunity and inflammation put people at risk for infection, disease, and cancer
35
Q

$ Categories of Hypersensitivity reactions

A
  1. Type I hypersensitivity (immediate)
  2. Type II hypersensitivity (tissue specific— hemolysis reactions to drugs)
  3. Type III hypersensitivity (immune complex- mediated)
  4. Type IV hypersensitivity ( delayed type, cell mediated)
36
Q

$ Type I Hypersensitivity
(Immunoglobulin E mediated)

A

-Allergic reactions to environmental allergens
-immediate reaction mediated by IgE
-IgE binds to mast cells —> mast cells degranulate—> histamine is released -when re exposed to allergen, cross linking of IgE antibodies triggers release of inflammatory mediators (rapid onset of symptoms mins to hours)
-Systemic response:
1. Vasodilation (redness/ hypotension)
2. Increased vascular permeability (edema)
3. Smooth muscle contraction (bronchus constriction)
-Treatment: antihistamines, corticosteroids, epi pen
-Ex: hives, asthma, anaphylaxis

37
Q

Two type of histamine receptors

A
  1. H1 in the lungs (pro inflammatory and first to respond to allergic reactions)
    -why you have the resp symptoms you see
  2. H2 in the GI tract (comes along later to decrease the inflammatory response and knocks down the allergic response)
38
Q

$ Type III hypersensitivity
(Immune complex mediated)

A

-Prime examples: systemic lupus erythematosus (SLE)/ RA/ glomerulonephritis
-Occurs when immune complexes (formed by antigen- antibody binding) deposit in tissues and activate complement, leading to an overwhelm of neutrophils to phagocytize and lysosomes are released into the tissue
-can manifest hours to days after exposure to antigen
-“auto” immune because the DNA deposits are the individuals own DNA
-Diagnosis: Antinuclear antibodies must be positive (ANA +)

39
Q

Systemic Lupus Erythematosus (SLE)

A

-Type III hypersensitivity reaction
- positive ANA
-Has remission and exacerbations
-Tissue deposits are systemic but usually
Found in the kidneys (vasculitis), connective tissues (arthritis), heart and brain (complexes that breach BBB)
-Damage is cumulative and progressive
-No cure—> immunosuppressants, steroids, anti inflammatories

40
Q

$ Type IV hypersensitivity reaction
(Delayed type)

A

-Involve sensitized T cells (CD4 and CD8) recognizing antigens and releasing cytokines that recruit and activate immune cells, leading to tissue damage
-Typically develop over 24-72 hours after exposure
-Ex: contact dermatitis (poison ivy) graft rejection, multiple sclerosis
-Treatment: topical steroids, immunosuppressants, and avoiding triggering antigens

41
Q

$ Transplant rejection

A

-Major histocompatibility molecules activation—> lymphocytes activated —> CD4 helper cells increase inflammation and cause activation of CD8 cytotoxic cells—> causes direct cell damage

-Rejection occurs when recipient develops antibodies to donor antigen

-Acute rejection: recipient lymphocytes interact with donor dendritic cells—> triggers cytokines—> activates macrophages and CD8 cells

-Chronic rejection: ongoing inflammation and damage to endothelial cells of transplant (antibodies against HLA activate the compliment and cytotoxic, low slow build over time)

42
Q

Covid 19

A

-Stimulates innate and adaptive system
-Innate response: Cytokines and chemokines unregulated—> significant inflammatory response
-Adaptive response: novel antigen, no initial adaptive response but over time generate T and B cell activation, generated IgG and IgM (can measure antibody levels to measure memory both after infection and vaccination)

43
Q

$ Physiologic effects on the immune system

A
  1. Stress:
    -can lead to a decrease in circulating B and T cells
    -can dysregulate the immune response (making you more susceptible to infection/ inflammation)
  2. Nutrition:
    -poor nutrition can result in lower B and T cells
    -malnutrition leads to immune deficiencies
    -low zinc (crucial for development and function of immune cells)
    -low vitamin b 12 (decreased WBC production and impaired T/B cells)
    -low vitamin a, c, e (lacking vital antioxidants that play a role in immune function)
  3. Cancer:
    -can dysregulate immune system by producing cytokines
    -can further nutritional deficiencies
  4. Immunosuppression
    -Targets T cells, leading to a weakened immune response (increases susceptibility to infection/ cancer/ autoimmune disease)

Advanced Patho Test 1 (20 decks)

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