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Questions and Answers

What is the significance of the class switching from IgA to IgG in patients with serious anaphylactic allergies?

The class switching allows for a more effective immune response without altering the antibody's antigen specificity, which is crucial in managing severe allergic reactions.

How do Th1 and Th2 cells differ in their roles during the immune response?

Th1 cells are involved in cell-mediated responses against intracellular pathogens and produce cytokines like IFNy and IL-2, while Th2 cells respond to allergic reactions and produce IL-4, IL-5, and IL-13, activating B cells for IgE production.

What is the role of TCR in T-cell activation and how does it interact with MHC molecules?

TCR is crucial for antigen recognition, binding specifically to MHC molecules to initiate the signaling cascade necessary for T-cell activation.

In what way does the immune system maintain tolerance to self-antigens?

The immune system is unresponsive to self-antigens through the positive and negative selection of lymphocytes during their development. Signup and view all the answers

What mechanisms are involved in Type 1 and Type 2 hypersensitivity reactions?

Type 1 hypersensitivity involves immediate allergic responses mediated by IgE and histamines, while Type 2 hypersensitivity involves IgG and IgM antibodies targeting cells or tissues, leading to their destruction. Signup and view all the answers

What is the primary function of central tolerance in the immune system?

Central tolerance primarily eliminates self-reactive lymphocytes in the thymus and bone marrow to prevent autoimmunity. Signup and view all the answers

How do peripheral tolerance mechanisms prevent the activation of self-reactive T cells?

Peripheral tolerance prevents activation through mechanisms such as anergy, deletion, or immunological ignorance. Signup and view all the answers

What role do regulatory T cells (Treg) play in immune tolerance?

Treg cells suppress the activation of self-reactive T and B cells, thereby maintaining immune tolerance. Signup and view all the answers

Describe the process of apoptosis in lymphocytes regarding immune tolerance.

Apoptosis in lymphocytes can be induced by pro-apoptotic proteins following antigen recognition, leading to caspase activation. Signup and view all the answers

What is clonal anergy, and how does it contribute to immune tolerance?

Clonal anergy refers to the functionally unresponsive state of T cells that recognize self-antigens without adequate co-stimulation. Signup and view all the answers

Identify two potential causes of autoimmunity as mentioned in the content.

Autoimmunity can arise from the loss of tolerance and the formation of new epitopes. Signup and view all the answers

Explain the significance of genetic and environmental factors in the development of autoimmune diseases.

Genetic factors can lead to forbidden clones of self-reactive cells, while environmental triggers such as infections may activate these cells. Signup and view all the answers

What is the role of CTLA-4 and PD-1 molecules in maintaining immune tolerance?

CTLA-4 and PD-1 dampen the immune response by inhibiting T cell activation. Signup and view all the answers

How does the recognition of self antigens lead to suppression by lymphocytes?

Self-antigen recognition activates Tregs, which then suppress the activation of other lymphocyte subsets. Signup and view all the answers

What triggers the activation of caspases during lymphocyte apoptosis?

The activation of caspases is triggered by the leakage of mitochondrial proteins and pro-apoptotic signaling upon antigen recognition. Signup and view all the answers

What role do non-self reactive lymphocytes play in the immune system?

They may become active in response to stimuli from the innate immune system. Signup and view all the answers

How does systemic lupus erythematosus affect various body systems?

It causes the body to attack connective tissue, impacting organs like the heart, lungs, and kidneys. Signup and view all the answers

What is the main pathogenic mechanism of rheumatoid arthritis?

The immune system attacks the joint synovium, resulting in inflammation that destroys cartilage. Signup and view all the answers

Describe the impact of type 1 diabetes on pancreatic function.

It leads to the destruction of pancreatic beta cells, impairing insulin secretion. Signup and view all the answers

What is the autoimmune mechanism behind pemphigus vulgaris?

It involves the production of autoantibodies against desmoglein-3, disrupting cell adhesion. Signup and view all the answers

How is Sjogren’s syndrome classified and what systems does it affect?

It is classified as primary or secondary and affects exocrine glands, particularly salivary and lacrimal glands. Signup and view all the answers

What are the challenges in managing an immunocompromised patient?

They face recurrent infections and conditions like oral candidiasis due to weakened immunity. Signup and view all the answers

How does the treatment plan for Sjogren’s syndrome aim to alleviate symptoms?

It focuses on relieving symptoms, replacing secretions, and suppressing the immune system. Signup and view all the answers

What is the significance of autoantibodies in diagnosing rheumatoid arthritis?

Autoantibodies directed to IgEFc serve as key markers in the diagnosis of rheumatoid arthritis. Signup and view all the answers

What are the clinical signs of benign mucous membrane pemphigoid?

Clinical signs include red inflamed gingiva and subepithelial clefting. Signup and view all the answers

Study Notes

Antibody Isotype Switching

The process of altering the constant region of an antibody without changing its antigen specificity.
This switching is regulated by the cytokine environment.
Important for patients with anaphylactic allergies.

T Helper Cell Subsets

Th0: Undifferentiated CD4+/CD8+ cells, no cytokines produced (naive T cells).
Th1: Subsets of CD4+, produced during cell-mediated responses (parasites, viruses, bacteria).
- Secrete cytokines like IFNγ and IL-2.
Th2: Subsets of CD4+, produced during allergic responses.
- Secrete cytokines like IL-4, 5, and 13.
- Activates and differentiates B cells into plasma cells, leading to IgE production.
- Particularly active against parasites.

TCR and MHC in T Cell Activation

TCR: Responsible for antigen recognition.
- Binds to specific MHC complex, initiating signaling cascade for T cell activation.
MHC Class 1: Presents peptides to CD8+ cells on nucleated cells.
MHC Class 2: Presents peptides to CD4+ cells on antigen-presenting cells (APCs).
- Both MHC classes lead to TCR activation if the antigen is recognized.

Immune Response

Achieved through interactions between TCR and BCR.
The immune system is unresponsive to self-antigens.
- Constantly generates lymphocytes that recognize self-antigens, ensuring tolerance.
Unresponsive to harmless external bacteria or commensal organisms.

Central vs Peripheral Tolerance

Central Tolerance:
- Occurs in the thymus and bone marrow.
- Immature lymphocytes undergo negative selection to eliminate self-reactive cells before entering the circulation.
- Mechanisms include deletion, apoptosis, receptor editing (changing antigen specificity), and differentiation into Treg cells.
Peripheral Tolerance:
- Occurs after T cells exit the thymus or B cells exit the bone marrow.
- Limits activation of mature self-reactive T cells through:
  - Anergy (functional inactivation).
  - Deletion.
  - Immunological ignorance (ignoring self-antigens).
- Controlled by Treg cells, B cells, and other leukocytes.
- Molecules like CTLA-4 and PD-1 on T cells help maintain tolerance.

Mechanisms of Peripheral Tolerance

Apoptosis:
- Induced by pro-apoptotic proteins.
- Antigen recognition triggers:
  - Production of pro-apoptotic proteins.
  - Leakage of mitochondrial proteins.
  - Activation of cytosolic enzymes (caspases) in the absence of co-stimulation.
  - Co-expression of death receptors which trigger pro-apoptotic protein production.
Clonal Anergy:
- Functionally unresponsive state.
- Occurs when self-antigen recognition lacks adequate co-stimulation or TCR complex signaling.
- Inhibitory signals from receptors other than the TCR complex can induce anergy.
- Mechanisms involve:
  - Activation of enzymes like ubiquitin ligases.
  - Modification of signaling proteins, leading to their destruction or stimulation of inhibitory proteins.
Suppression:
- Development of suppressor cells.
- Lymphocyte subsets act as suppressors or regulators of T and B cell activation.
- Recognition of self-antigens leads to the activation of suppressor cells which suppress the activation of lymphocytes specific for these self-antigens.
- Types of suppressor cells include CD4+ T regulatory cells (Treg) and CD8+ T suppressor cells (Ts).

Autoimmunity

May arise from loss of tolerance, formation of new epitopes, exposure of hidden epitopes, or epitope sharing.
Severity and development depend on genetic makeup.
Genetic factors: Formation of forbidden clones (self-reactive lymphocytes).
Environmental triggers: Infections (viral or bacterial).
- Autoantibodies can aid in diagnosis.
Cell-mediated response:
- Non-self-reactive lymphocytes may become active.
- Innate immune system can activate mature lymphocytes, initiating an adaptive immune response that can damage the body's own tissues.

Autoimmune Disorders

Systemic Lupus Erythematosus (SLE):
- Chronic autoimmune disease affecting connective tissue in the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system.
- Characterized by unpredictable flares.
- Symptoms include butterfly facial rash.
- Medications include immunosuppressants.
- Oral implications: Predisposition to infections, pain, and swelling.
Rheumatoid Arthritis (RA):
- Chronic systemic inflammatory disorder that attacks the synovium of joints, leading to thickening and destruction of cartilage and joints.
- Can also affect lungs, heart, pericardium, vessels, pleura, sclera, neurological system, and skin.
- Individuals with HLA-DRA allotypes of MHC class II are more susceptible to RA.
- Autoantibodies directed to IgE Fc are used for diagnosis.
Diabetes Mellitus Type 1:
- Autoimmune destruction of pancreatic beta cells, leading to insulin deficiency.
- Involves inflammation of the islets of Langerhans.
- Normal secretion of glucagon, somatostatin and pancreatic polypeptide.
- Characterized by a large number of mononuclear cells and CD8+ T cells targeting beta cells.
Pemphigus Vulgaris:
- Autoimmune disease targeting skin and oral mucosa desmosomes.
- The immune system produces autoantibodies against desmoglein-3, leading to cell detachment.
- Clinical signs: Ulcerations and shedding of the buccal mucosa and gingival ulceration.
Benign Mucous Membrane Pemphigoid:
- Production of autoantibodies against the basement membrane of the oral mucosa.
- Clinical signs: Red, inflamed gingiva and subepithelial clefting.
Sjogren's Syndrome:
- Autoimmune disorder that primarily affects exocrine glands (primary Sjogren's) or in conjunction with connective tissue diseases (secondary Sjogren's).
- Autoantigens in salivary and lacrimal glands are recognized as foreign by the immune system, leading to activation of CD4+ and B cells.
- Activated lymphocytes release cytokines and chemokines, resulting in inflammation and tissue damage.
- Targets and destroys salivary ducts and acinar cells.
- Oral implications:
  - Lacrimal gland: Epithelial cell death and disintegration, leading to dry eyes, photosensitivity, and foreign body sensation.
  - Salivary gland (xerostomia): Speech difficulties, chewing and swallowing problems, altered taste, pain, burning, cracked and dry lips, fissures, gland swelling, rampant caries, occlusal wear, mucositis, and chronic candidiasis.
- Treatment:
  - Relieving symptoms.
  - Replacing secretions (insulin, thyroid hormone, synthetic tears, saliva replacement).
  - Suppressing the immune system (immunosuppressants, anti-inflammatory medications, chemotherapy, anti-TNF).

Immunodeficiency (ID)

Immunocompromised state that impacts health and oral health.
Oral health impacts: Oral candidiasis and recurrent infections.
Primary ID: Present at birth, caused by defects in the immune system.
Secondary ID: Acquired through external factors (injections, malnutrition, medications).
- Immunosuppressive drugs are prescribed to suppress the immune system, helping prevent tissue rejection in transplant patients.