TEST 2: Immunity Flashcards
$ Innate Immunity (nonspecific response)
-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
$ Adaptive Immunity (acquired)
-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
Antibody response in Innate Vs. Adaptive Immunity
-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
$ Antigen
(ANYTHING foreign to your body)
-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
$ Haptens
-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
$ Antibody
Aka “Immunoglobulin”
-Glycoproteins produced by B lymphocytes in response to the presence of antigens
-Classified as IgG, IgM, IgE, IgA, IgD
$ Short term immunoglobulin
(IgM)
-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
$ Long term immunoglobulin
(IgG)
-The main antibody class responsible for long term immunity
-Provides lasting protection against pathogens and enhances immune memory
$ Antigen Presenting Cell
(APC)
-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
Structure of Immunoglobulins
Aka antibodies
-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
Immunoglobulin A (IgA)
-Found mainly on mucosal areas like resp/ GI tract
-Crucial role in mucosal immunity and defense
Immunoglobulin M (IgM)
-FIRST antibody produced in response to infection
-Involved in primary immune response and acts as potent activator of complement system
Immunoglobulin G (IgG)
-Most abundant antibody in bloodstream
-Provides long term immunity
-Can cross the placenta
-Key role in immune memory
Immunoglobulin E (IgE)
-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
Immunoglobulin D (IgD)
-Found mainly on the surface of B cells, where to functions as a receptor for antigen recognition
-Involved in B cell activation and maturation
$ Generic T vs. B cells
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
$ T Cells
-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.
$ B Cells
-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
Lymphocytes in waiting
-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
$ T cell maturation
-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
$ B cell maturation
-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
$ B cell response
-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
$ Antibodies overview
-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)
$ 4 ways antibodies provide protections from antigens overview
- Neutralization: prevents antigens from exerting harmful effects
- Opsonization: enhances phagocytosis of antigens by immune cells
- Agglutination: facilitates removal of antigens by clustering them together
- Precipitation: aids in the clearance of insoluble antigens from the body
Direct effects antibodies have on antigens
-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
$ Indirect effect antibodies have on antigens
-Activation of the innate immune response
-IgM: activate the complement system
-IgA: Opsonization
$ Two types of adaptive immunity
- Acquired (active)
- Passive
Acquired (active) immunity
-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
$ Passive immunity (acquired)
-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
$ Acquired (active) immunity vs. passive immunity (both are adaptive)
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
$ Key time periods for fetal/ newborn immunity
- 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)
- T and B cell production: begins are 6-8 months after birth (significant milestone in building babies immunity)
- Weak leukocytes at birth: are weak and less lethal at birth, making newborns more susceptible to infection until immune system strengthens over time
- 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).
Major Histocompatibility complex
-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
Secretory immune response In mucosal system (acquired adaptive response)
-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)
$ Age related immune transitions
- T cells: less likely to make more, leading to a weakened adaptive response
- B cells: number remains stable, but less responsive to new antigens, leading to a reduced ability to mount robust immune responses
- Chronic inflammation: tendency for immune system to be chronically activated leading to increased inflammation (aka “inflammaging”) sustained response can contribute to disease development
- 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
$ Categories of Hypersensitivity reactions
- Type I hypersensitivity (immediate)
- Type II hypersensitivity (tissue specific— hemolysis reactions to drugs)
- Type III hypersensitivity (immune complex- mediated)
- Type IV hypersensitivity ( delayed type, cell mediated)
$ Type I Hypersensitivity
(Immunoglobulin E mediated)
-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
Two type of histamine receptors
- H1 in the lungs (pro inflammatory and first to respond to allergic reactions)
-why you have the resp symptoms you see - H2 in the GI tract (comes along later to decrease the inflammatory response and knocks down the allergic response)
$ Type III hypersensitivity
(Immune complex mediated)
-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 +)
Systemic Lupus Erythematosus (SLE)
-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
$ Type IV hypersensitivity reaction
(Delayed type)
-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
$ Transplant rejection
-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)
Covid 19
-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)
$ Physiologic effects on the immune system
- Stress:
-can lead to a decrease in circulating B and T cells
-can dysregulate the immune response (making you more susceptible to infection/ inflammation) - 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) - Cancer:
-can dysregulate immune system by producing cytokines
-can further nutritional deficiencies - Immunosuppression
-Targets T cells, leading to a weakened immune response (increases susceptibility to infection/ cancer/ autoimmune disease)
