Quiz 4 Review

How do vaccine prevent disease

• expose the immune system to antigens,

• producing protective adaptive immunity and memory cells without requiring natural infection.

immunological memory

The ability of memory B and T cells to respond faster and more effectively upon reexposure to the same pathogen.

How long do primary and secondary adaptive immune responses take?

Primary: up to 14 days (slow). Secondary: approximately 3–4 days (fast).

secondary immune response stronger

Memory B cells rapidly produce high-affinity antibodies

• have undergone somatic hypermutation and isotype switching.

clonal selection and expansion

To activate and multiply antigen-specific lymphocytes, producing effector and memory cells.

what must vaccine do?

• must induce a primary immune response that promotes activation of the exact lymphocytes needed to combat the actual pathogen

What are live attenuated vaccines?

Vaccines containing weakened pathogens that can replicate and stimulate strong immune responses.

inactivated vaccines

vaccines containing killed or inactivated pathogens that cannot replicate but still stimulate immunity.

toxoid vaccine

Vaccines containing inactivated bacterial toxins that stimulate toxin-neutralizing antibodies.

subunit vaccines

Vaccines containing selected pathogen antigens rather than the entire pathogen.

• Neutralize antibodies can bind to adhesion molecules of intracellular pathogen

conjugate vaccines

Vaccines linking bacterial polysaccharides to protein carriers to promote T-cell help and antibody production.

• Joins weak antigen to strong antigen to make multivalent vaccines with multiple epitopes

recombinant vector vaccines

Vaccines using a modified carrier organism to deliver genes encoding pathogen antigens.

• Uses harmless bacteria or attenuated viruses for pathogenic antigen which elicits adaptive response

how do DNA and mRNA vaccines work

They deliver genetic instructions that allow host cells to produce pathogen antigens and stimulate adaptive immunity.

adjuvant

To strengthen vaccine-induced immune responses by promoting inflammation and immune activation.

How do adjuvants improve T-cell activation?

They stimulate antigen-presenting cells to express costimulatory molecules such as B7.

Which costimulatory interaction is important during vaccination?

B7 on antigen-presenting cells binds CD28 on T cells to promote activation.

Why is inflammation important during vaccination?

It promotes expression of costimulatory molecules on antigen-presenting cells.

Which costimulatory molecule is expressed by activated dendritic cells?

B7.

Which T-cell receptor interacts with B7 to provide costimulation?

CD28.

What happens if a naïve T cell recognizes antigen without proper costimulation?

It may become anergic, meaning functionally unresponsive.

two major processes must an effective vaccine promote

• Clonal selection

• expansion of protective lymphocytes, plus proper costimulation.

Type I hypersenstivity

Allergens cross-link IgE bound to FcεRI on mast cells and other granulocytes, triggering degranulation.

Which antibody and immune cells are involved in Type I hypersensitivity?

IgE; mast cells, basophils, and eosinophils.

What happens during the first and second allergen exposures?

• First: sensitization and IgE production.

• Second: allergen cross-linking of IgE triggers degranulation.

Which inflammatory mediators are released during Type I hypersensitivity?

Histamine, leukotrienes, prostaglandins, heparin, and TNF-α.

What are examples of Type I hypersensitivity?

Allergic rhinitis, asthma, food allergies, hives, and anaphylaxis.

anahylatic shock

• Widespread mast-cell activation

• causes vasodilation, vascular leakage, decreased blood pressure, and possible airway obstruction.

What causes Type II hypersensitivity?

IgG or IgM binds cell-surface antigens

• causing complement activation, opsonization, or ADCC.

What are examples of Type II hypersensitivity?

Incompatible blood transfusions and hemolytic disease of the newborn.

What are the three major mechanisms of Type II hypersensitivity?

• Opsonization and phagocytosis,

• complement activation,

• antibody-dependent cellular cytotoxicity (ADCC).

What is antibody-dependent cellular cytotoxicity (ADCC)?

Immune cells recognize antibody-coated target cells through Fc receptors and destroy them.

What is an example of Type II hypersensitivity involving blood transfusions?

An incompatible transfusion causes antibodies to target donor red blood cells.

What is hemolytic disease of the newborn?

Maternal antibodies attack fetal red blood cells, such as in Rh incompatibility.

Why is the first Rh-positive pregnancy often less affected?

The Rh-negative mother is usually sensitized during fetal blood exposure late in pregnancy or childbirth.

What happens during a later Rh-positive pregnancy after sensitization?

Maternal anti-Rh IgG can cross the placenta and destroy fetal red blood cells.

Why is the first Rh-positive pregnancy often less affected?

The Rh-negative mother is usually sensitized during fetal blood exposure late in pregnancy or childbirth.

What happens during a later Rh-positive pregnancy after sensitization?

Maternal anti-Rh IgG can cross the placenta and destroy fetal red blood cells.

What causes Type III hypersensitivity?

IgG binds soluble antigens, forming immune complexes that activate complement and inflammatory cells.

immune complex

An antigen bound to antibodies.

Which immune cells contribute to tissue damage in Type III hypersensitivity?

Phagocytes, especially neutrophils.

What are examples of Type III hypersensitivity?

Serum sickness (systemitic)  and the Arthus reaction (localized). Both being immune complex mediated inflammatory reaction

What causes Type IV hypersensitivity?

Delayed activation of antigen-specific T cells, resulting in inflammation and tissue damage.

What are examples of Type IV hypersensitivity?

Contact dermatitis and granuloma formation.

Which immune cells are primarily responsible for Type IV hypersensitivity?

T lymphocytes rather than antibodies.

which cytokine activates macrophages during Type IV hypersensitivity?

IFN-γ.

What is the role of activated macrophages in Type IV hypersensitivity?

They produce inflammatory responses that can damage surrounding tissues.

what are examples of Type IV hypersensitivity?

Contact dermatitis and granuloma formation.

What effects can mast-cell degranulation cause?

Increased vascular permeability, smooth muscle contraction, and inflammation.

What is anaphylaxis?

A severe systemic allergic reaction involving widespread mast-cell activation, vasodilation, and potentially shock.

self tolerance

The immune system's ability to avoid attacking the body's own antigens.

autoimmunity

An immune response against self-antigens due to failure of self-tolerance.

What are the two major mechanisms of self-tolerance?

Central tolerance and peripheral tolerance.

centeral tolerance

Elimination of developing self-reactive T and B cells through negative selection in primary lymphoid tissues.

peripheral tolerance

Prevention of self-reactive lymphocyte activation through anergy, regulatory T cells, and costimulatory requirements.

anergy

A state of functional unresponsiveness when a lymphocyte does not receive appropriate activation signals.

How do regulatory T cells prevent autoimmunity?

They suppress activation and activity of potentially self-reactive T cells.

What happens when central or peripheral tolerance fails?

Autoreactive lymphocytes can become activated and attack the body's own tissues.

What is the difference between organ-specific and systemic autoimmunity?

Organ-specific autoimmunity targets particular tissues, while systemic autoimmunity affects multiple organs.

How do genetic factors contribute to autoimmune disease?

Certain inherited MHC polymorphisms increase susceptibility by presenting self-antigens to autoreactive T cells.

How do environmental factors contribute to autoimmune disease?

Chemical exposure and physical trauma can increase the risk of autoimmune responses.

What is the role of AIRE in preventing autoimmunity?

AIRE promotes expression of tissue-specific proteins in the thymus for negative selection of autoreactive T cells.

What happens if AIRE does not function properly?

Autoreactive T cells may escape negative selection and contribute to autoimmune disease.

How can failure of T-cell negative selection cause autoimmunity?

Self-reactive T cells survive development and may attack the body's tissues.

How does the B7-CD28 interaction help prevent autoimmunity?

It ensures T cells require a proper costimulatory signal before activation.

What happens when a T cell recognizes self-antigen without costimulation?

It normally becomes anergic, preventing an autoimmune response.

What is the role of CTLA-4 in preventing autoimmunity?

CTLA-4 binds B7 and inhibits excessive T-cell activation.

How can defective regulatory T cells contribute to autoimmunity?

They fail to suppress autoreactive lymphocytes, allowing immune attacks against self-tissues.

How can autoreactive T cells promote autoantibody production?

They activate autoreactive B cells, which differentiate into plasma cells that produce autoantibodies.

Why are endocrine glands susceptible to autoimmune disease?

highly vascularized and express specialized tissue-specific proteins that can become autoimmune targets.

How can loss of central tolerance affect endocrine glands?

Failure to present endocrine tissue-specific antigens during development allows autoreactive lymphocytes to survive.

Which two endocrine organs are emphasized as autoimmune targets?

The pancreas and thyroid.

What causes type 1 diabetes mellitus?

Autoimmune destruction of insulin-producing pancreatic β cells.

Where are pancreatic β cells located?

In the islets of Langerhans.

Which pancreatic cells produce glucagon?

Pancreatic α cells.

Which pancreatic cells produce insulin?

Pancreatic β cells.

What pancreatic β-cell antigens can be targeted in type 1 diabetes?

insulin, glutamate decarboxylase, and IA-2 protein.

What causes Graves disease?

Autoantibodies stimulate TSH receptors on thyroid cells, increasing T3 and T4 production.

Do Graves disease autoantibodies act as agonists or antagonists?

Agonists; they mimic TSH and stimulate the receptor.

Does Graves disease cause hyperthyroidism or hypothyroidism?

Hyperthyroidism.

What are common symptoms of Graves disease?

Heat intolerance, weight loss, excessive sweating, and warm skin.

What causes Hashimoto disease?

Autoimmune destruction of thyroid epithelial cells, including through antibody-dependent cellular cytotoxicity.

Does Hashimoto disease cause hyperthyroidism or hypothyroidism?

Hypothyroidism.

Which thyroid proteins are recognized by autoantibodies in Hashimoto disease?

Thyroid peroxidase, thyroglobulin, and the TSH receptor.

What are common symptoms of Hashimoto disease?

Fatigue, weight gain, hair loss, dry skin, and cold intolerance.

What is the major similarity between hypersensitivity and autoimmune diseases?

Both involve immune responses that can cause inflammation and tissue damage.

What is the major difference between hypersensitivity and autoimmunity?

Hypersensitivity involves harmful responses to antigens, often foreign; autoimmunity specifically targets self-antigens.

Which hypersensitivity mechanisms commonly resemble autoimmune disease?

Type II antibody-mediated and Type III immune complex-mediated reactions.

How does Type II hypersensitivity resemble autoimmune disease?

Antibodies recognize tissue antigens and cause damage through complement or ADCC.

What is Goodpasture syndrome?

autoimmune disease in which antibodies attack basement membranes of the kidneys and lungs.

Which hypersensitivity type resembles Goodpasture syndrome?

Type II hypersensitivity.

Why does Hashimoto disease resemble Type II hypersensitivity?

Autoantibodies contribute to destruction of thyroid cells through ADCC.

How does Type III hypersensitivity resemble autoimmune disease?

Immune complexes deposit in tissues and activate complement and inflammatory cells.

Which autoimmune diseases can involve Type III-like immune complex reactions?

Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

What immune effector mechanisms are shared by hypersensitivity and autoimmunity?

Complement activation, ADCC, inflammation, and immune complex-mediated responses.

What are autoantibodies?

Antibodies produced by autoreactive B cells that recognize the body's own antigens.

How can autoantibodies cause autoimmune disease?

They can activate or block receptors, promote cell destruction, or form inflammatory immune complexes.

What is an agonist autoantibody?

An antibody that activates a receptor by mimicking its normal ligand.

What is an antagonist autoantibody?

An antibody that blocks a receptor and prevents normal signaling.

How do autoantibodies cause Graves disease?

They act as TSH receptor agonists, stimulating excessive thyroid hormone production.