Immunology Exam 2

What are mucins?

Large glycoproteins secreted by epithelial cells that give mucus its viscosity and protective properties.

What are commensal bacteria?

Microorganisms that live in the gut in a symbiotic relationship with the human host.

What are the 5 main benefits of commensal bacteria in the gut?

1. Synthesize essential metabolites.

2. Break down plant fibers.

3. Inactivate toxic substances.

4. Prevent pathogens from benefiting from the resources of the human gut

5. Interact with the epithelium to trigger development of secondary lymphoid tissue

What are the two functionally distinct compartments of GALT?

The inductive compartment and the effector compartment.

What is the inductive compartment of GALT?

Lymphoid tissue directly beneath the mucosal epithelium, where antigens interact with dendritic cells and lymphocytes.

What is the effector compartment of GALT?

The underlying connective tissue called the lamina propria.

What is the function of the lamina propria?

It contains resident immune effector cells that help defend mucosal tissues.

What are Peyer's patches?

Gut-associated secondary lymphoid tissues that help sample antigens and initiate adaptive immune responses.

What is the role of mesenteric lymph nodes?

They respond to infection after pathogens invade gut tissue and antigens are carried to the nodes through draining lymph.

What is the role of secondary lymph nodes?

continually sample and monitor gut lumen, enabling adaptive immune responses before a pathogen invades tissue

What happens to mesenteric lymph nodes without a microbiota?

They become underdeveloped.

What happens to Peyer's patches without a microbiota?

They become underdeveloped.

What happens to isolated lymphoid follicles without a microbiota?

Their numbers decrease.

How does the absence of microbiota affect secretory IgA and serum immunoglobulin?

Reduction in secretory IgA and serum immunoglobulin

How does the absence of microbiota affect systemic T cells?

Systemic T-cell numbers and activation decrease.

How does the absence of microbiota affect CD8 T cells?

Their cytotoxicity decreases.

How does the absence of microbiota affect lymphocytes in mucosal tissues?

Their numbers decrease.

What is the main characteristic of a typical non-mucosal inflammatory response?

Macrophages produce inflammatory cytokines, leading to inflammation that can damage tissue.

What happens when bacteria enter tissue through a surface wound in non-mucosal immunity?

Macrophages are activated and release inflammatory cytokines, triggering an inflammatory response.

What may happen to tissue after a non-mucosal infection is terminated?

The tissue is damaged or distorted and require repair.

How do intestinal epithelial cells contribute to innate immunity?

They act as a barrier and detect invading microorganisms, releasing cytokines and chemokines that recruit neutrophils and monocytes.

How do intestinal macrophages differ from blood monocytes?

Intestinal macrophages retain phagocytosis and killing abilities but have reduced inflammatory functions, including reduced cytokine production and chemotaxis.

Function of mucus

It traps microorganisms and particles, helping prevent them from reaching the epithelial surface.

What are M cells responsible for?

Transporting microbes and antigens from the gut lumen to the underlying gut-associated lymphoid tissue.

How are secretory IgA and IgM delivered to the gut lumen?

Through transcytosis across epithelial cells.

How do secretory IgA and IgM protect the gut?

They bind microorganisms and attach to mucus, helping prevent pathogens from reaching and invading the mucosal surface.

How can IgA remove pathogens or toxins from the lamina propria?

IgA binds pathogens, antigens, or toxins and carries them into the gut lumen through transcytosis.

What is the difference between IgA1 and IgA2?

-IgA1 has a longer hinge region but is more susceptible to proteolytic cleavage

-IgA2 has a shorter hinge region and is less susceptible.

Why is IgA2 more common than IgA1 in the colon?

The colon has high levels of proteases, and IgA2 is less susceptible to proteolytic cleavage.

What is the pathway for gut-homing effector T cells described in the lecture?

Peyer's patch activation → lymph → mesenteric lymph node → blood → mucosal tissue.

What is the significance of activating lymphocytes in mucosal tissues?

Activation in one mucosal tissue commits them to defending mucosal tissues more broadly.

How do effector T cells return to mucosal tissues?

After activation in mucosal tissue, they travel through lymph and blood and are directed back to mucosal sites as effector cells.

Where do activated effector T cells travel after leaving Peyer's patches?

They travel through lymph, pass through the mesenteric lymph nodes, and then enter the blood.

What happens to naïve T cells in Peyer's patches after antigen recognition?

They become activated, proliferate, and differentiate into effector T cells.

Where can gut antigens enter GALT to initiate an adaptive immune response?

Through M cells into Peyer's patches.

How do bacteria enter the tissue in the mucosal response?

They cross the gut epithelium and enter the lamina propria.

How do intestinal macrophages respond to bacteria?

They phagocytose and kill pathogens while limiting inflammatory cytokine production.

What is the role of dendritic cells during a mucosal infection?

They travel to mesenteric lymph nodes and help activate adaptive immunity.

What is the outcome of the mucosal response?

Infection is eliminated with little tissue damage and potentially no need for repair.

What happens after antigen-specific B and T cells are activated?

Effector cells return to the infected area to help eliminate the bacteria.

What is autoimmunity?

An adaptive immune response directed against self-antigens.

What is an autoantigen?

An antigen found on or in the body's own cells.

What is an autoantibody?

An antibody that recognizes and binds a self-antigen.

What is self-tolerance?

Mechanisms that prevent immune attacks against the body's own tissues.

What causes autoimmune disease?

An immune response against self-antigens that causes tissue pathology.

What defines a Type II autoimmune response?

IgG or IgM binds cell-surface or extracellular matrix antigens.

What defines a Type III autoimmune response?

Antibody-antigen immune complexes form and deposit in tissues.

What defines a Type IV autoimmune response?

-CD4: delayed type hypersensitivity (DTH)

-CD8: target-cell cytolysis.

What causes pemphigus blisters?

IgG binds to desmogleins and disrupts keratinocyte adhesion.

What do desmogleins normally do?

Help keratinocytes adhere to one another at desmosomes.

How do Graves' autoantibodies work?

They mimic TSH and continuously stimulate the TSH receptor causing continuous thyroid release

How do methimazole and propylthiouracil treat Graves' disease?

They inhibit thyroid peroxidase and reduce thyroid hormone synthesis.

How does radioactive iodine treat Graves' disease?

It destroys overactive thyroid tissue

What do beta blockers do in Graves' disease?

Temporarily control symptoms.

What is the result of myasthenia gravis autoantibodies?

Impaired nerve-to-muscle signaling and muscle weakness.

What do most drugs target in myasthenia gravis?

C5 which ultimately prevents mac

How does pyridostigmine work in myasthenia gravis?

It inhibits acetylcholinesterase, allowing ACh to remain available longer.

Examples of type II autoimmune diseases

-pemphigus

-grave's disease

-myasthenia gravis

how are auto-antibodies passed from mother to child specifically in graves

mother with graves makes TSHR-specific IgG which crosses the placenta to the fetus and gives the infant graves resulting in temporary symptoms and overtime antibodies are degraded

What causes purpura in mixed cryoglobulinemia?

complexes of autoantigens and IgM that precipitate in tissues where the temp is lower than that of blood causing bleeding from small blood vessels

What is the immune mechanism of systemic lupus erythematosus (SLE)?

Autoantibodies form complexes with cellular antigens; complexes deposit and trigger inflammation.

What are three contributors to increased autoantigens in SLE?

Increased apoptosis, impaired clearance of apoptotic cells, and immune activation by nuclear material.

How can nuclear material promote autoantibody production in SLE?

It activates dendritic cells, which promote B-cell activation and autoantibody production.

Examples of type III autoimmune diseases

SLE and cryoglobulinemia.

Which pancreatic cells produce insulin?

β cells of the islets of Langerhans

How does Type 1 diabetes develop?

Autoimmune responses attack pancreatic beta cells, causing insulin deficiency.

What type of hypersensitivity is type 1 diabetes?

type II/IV

What does rituximab target for type 1 diabetes

CD20-expressing B cells.

What does teplizumab target for type 1 diabetes

CD3, a component of the T-cell receptor complex.

What are rheumatoid factors?

Autoantibodies directed against the Fc portion of human IgG.

What cytokine is targeted by etanercept and adalimumab?

TNF-α.

What does tocilizumab target?

The IL-6 receptor.

How does methotrexate work according to the lecture?

It inhibits enzymes that break down adenosine, a natural anti-inflammatory agent.

What are the three goals of autoimmune disease treatment?

Decrease symptoms, control the autoimmune process, and replace deficiencies.

What type of hypersensitivity is rheumatoid arthritis?

Type III/IV

Which drugs are calcineurin inhibitors?

Cyclosporine and tacrolimus.

What is the result of calcineurin inhibition?

Reduced NFAT activation and decreased IL-2 production.

Which drugs are costimulation blockers?

Abatacept and belatacept.

How do costimulation blockers work?

Block CD80/86 interaction with CD28, reducing T-cell activation.

Which drugs are mTOR inhibitors?

Sirolimus and everolimus.

How do mTOR inhibitors work?

Block mTOR signaling, reducing T-cell growth and proliferation.

Which drugs are antimetabolites?

Azathioprine and mycophenolate mofetil.

How do antimetabolites work?

They interfere with purine synthesis needed to make genetic material and block DNA synthesis.

Corticosteroids target

block NF-kB and AP-1

What type of immunity is associated with parasite defense and allergic reactions?

Th2 immunity

What happens when an allergen cross-links IgE on mast cells?

Intracellular signaling triggers mast-cell degranulation.

What is mast-cell degranulation?

Release of preformed inflammatory mediators, including histamine.

What is the role of IgE in allergic reactions?

IgE binds mast-cell receptors and enables allergen-triggered activation.

Why can a second allergen exposure trigger a rapid reaction?

Allergen-specific IgE is already bound to mast cells.

What is the role of eosinophils in allergic inflammation?

They release toxic mediators that can damage tissues.

What is allergic rhinitis?

Allergen-induced nasal mast-cell activation causing sneezing and a runny nose.

What happens during allergic asthma?

Mast-cell activation increases mucus and fluid secretion and causes bronchoconstriction and air is trapped in the lung.

What characterizes chronic asthma?

Persistent inflammation, mucus plugs, and airway hyperreactivity.

What is urticaria?

Raised, itchy skin swellings (hives) caused by mast-cell mediator release.

What is angioedema?

More diffuse swelling in deeper subcutaneous tissue.

How do food allergens trigger gastrointestinal symptoms?

They activate IgE-coated mucosal mast cells, causing fluid leakage and smooth-muscle contraction.

How do antihistamines work?

They interfere with histamine's effects at H₁ receptors, reducing itching and allergic inflammation.

Which antihistamine generation is generally more sedating?

First-generation antihistamines.

How do corticosteroids reduce inflammation?

They increase anti-inflammatory protein production and inhibit NF-κB and AP-1.

What does the glucocorticoid-receptor complex bind in the nucleus?

The glucocorticoid response element (GRE).