micro exam 1

Type I hypersensitivity is mediated by which antibody and effector cell?

IgE bound to mast cells (via Fc receptors) that cross-link and degranulate, releasing histamine, leukotrienes, prostaglandins; immediate onset after re-exposure

basophil

granules, allergy/parasite response, least abundant WBC

mast cell

granules with histamine, only in tissue (not blood)

eosinophil

parasite, allery, phagocyte, have granules

granulocytes

neutrophils, basophils, mast cells, eosinophils

non-granulocytes

monocyte, macrophages, dendritic cells

caloprotectin

starves microbes; common in oral epithalium and neutrophils

catheridins

lysosomal antimicrobial

IL-1

from macrophages, pro-inflammatory

IL-6

from macrophages and T cells, pro-inflammatory and B cell differentiation

TNF-alpha

from macrophages and T cells, pro-inflammatory, kill tumor cells

TGF-beta

from macrophages, lymphocytes, endothelial cells and platlets. IgA production, wound healing, suppress cytokine production

IFN-gamma

from T cells and NK cells, actiavte macrophages and NK cells, upregulate MHC 1 and 2 and inhibit T helper 2

IFN-alpha

from leukocytes, activate macrophages, NK cells, and upregulate MHC and anti-viral machinery

IL-17

from T cells, pro-inflammatory and hematopoesis

IL-10

from macrophages and T cells, inhibit cytokine productions, stops response/anti-inflammatory

IL-8

from macrophages, cause neutrophil chemotaxis

What is the sensitization step in Type I hypersensitivity?

Initial exposure to allergen induces IgE production; subsequent exposures trigger immediate mast cell degranulation

List common clinical examples of Type I hypersensitivity.

Anaphylaxis (life-threatening), allergic rhinitis, certain drug allergies, latex allergy

Define Type II hypersensitivity and give dental-relevant examples.

Antibody-mediated cytotoxicity targeting cell-bound antigens; examples: pemphigus vulgaris (oral blisters/erosions), Goodpasture syndrome (kidney), autoimmune hemolytic anemia (RBCs)

Pemphigus vulgaris vs mucous membrane pemphigoid—what is the target and where do lesions appear?

Pemphigus vulgaris: antibodies against desmosomes; skin and oral mucosa. Mucous membrane pemphigoid: antibodies against basement membrane; predominantly mucosal surfaces, less often skin

Define Type III hypersensitivity and list classic conditions.

Immune complex-mediated disease due to antigen-antibody complexes depositing in tissues and activating complement; examples: serum sickness, SLE (lupus), glomerulonephritis

Mechanism and timing overview for hypersensitivity types using "ACID."

A (Type I—Anaphylactic/allergy): IgE/mast cells, seconds-minutes. C (Type II—Cytotoxic): antibodies against cell antigens, hours-days. I (Type III—Immune complex): complexes deposit and activate complement, days-weeks. D (Type IV—Delayed): T-cell mediated, 48-72 hours

What defines Type IV (delayed) hypersensitivity, and what is a classic example?

T-cell mediated immune response with delayed onset (48-72 hours); classic example: poison ivy; oral lichenoid reactions can be similar in timing

Oral lichenoid reaction—what clinical timing and effector suggest the mechanism?

Perioral itching/rash appearing ~48 hours after new material exposure suggests Type IV (T-cell mediated) delayed hypersensitivity

Oral lichen planus vs candidiasis—how can you differentiate at chairside?

Oral lichen planus white lesions do not wipe off; candidal plaques typically wipe off with gauze

Define immunologic tolerance and its induction sites.

The state in which lymphocytes do not react to self antigens; induced in bone marrow (B cells) and thymus (T cells)

Autoimmunity—typical etiologic pattern?

Genetic susceptibility plus an environmental trigger (e.g., viral infection) leading to self-directed B- or T-cell responses

Example of autoimmune disease triggered by infection in a genetically susceptible host.

Type 1 diabetes mellitus: often follows viral infection leading to immune attack on pancreatic beta cells

Sjogren's syndrome—key oral and ocular clues and consequences.

Dry mouth (xerostomia), dry eyes; reduced saliva causes rampant caries and predisposes to oral candidiasis via impaired immune exclusion and dysbiosis

Beyond medications, what clinical cue points to Sjogren's rather than drug-induced xerostomia?

Concurrent dry eyes (keratoconjunctivitis sicca) indicating systemic exocrine gland involvement

As a dentist, how should you act upon suspected Sjogren's in a patient?

Recognize oral/ocular signs, manage caries/xerostomia symptoms, and refer to medical team for definitive evaluation and systemic management

If antibodies are deficient, which infections increase and why?

Extracellular bacterial infections increase; antibodies neutralize, opsonize, and target extracellular microbes without MHC presentation

If T cells are deficient, which infections increase and why?

Viral and opportunistic/fungal infections increase; T cells (especially CD8+) recognize infected cells via MHC I; T-cell help is needed for effective B-cell responses

If neutrophils are deficient, which infections increase?

Fungal infections and many bacterial infections; neutrophils are first responders critical for phagocytosis and killing

If complement is deficient, which infections are likely?

Bacterial infections, including risk for invasive Neisseria species due to impaired membrane attack complex and opsonization

Primary vs secondary immunodeficiency—key distinctions.

Primary: inherited defects (e.g., SCID) presenting early with severe/recurrent infections. Secondary: acquired (e.g., chemotherapy, immunosuppressive drugs, malnutrition, aging, chronic disease)

What classic primary immunodeficiency is associated with "boy in the bubble"?

Severe Combined Immunodeficiency (SCID)—profound deficiency of adaptive immunity leading to fatal infections without isolation/therapy

Recurrent oral candidiasis with weight loss and lymphadenopathy—what should a dentist consider and do?

Consider underlying immunodeficiency; order/coordinate referral for labs (CBC with differential, A1C if indicated) and medical evaluation; treat the fungus but also address root cause via referral

Transplant patients—what immune elements are matched and suppressed?

HLA/MHC matched; T-cell activation suppressed (e.g., tacrolimus) to prevent graft rejection

Dental management priorities for immunosuppressed transplant patients.

Review immunosuppressive meds and side effects (e.g., xerostomia), screen for infections, coordinate invasive care (extractions, periodontal surgery, crowns) with medical team, consider pertinent blood counts

Recognize-act safely framework in dental care for immune dysfunction—what are the steps?

Identify oral clues (lesions, dry mouth, meds), infer immune mechanism (infection risk, bleeding risk, airway risk in anaphylaxis), and coordinate/referral with the medical team before proceeding

Antibiotic allergy scenario—what is the appropriate action if you did not prescribe the antibiotic?

Do not change dose or class yourself; contact and refer back to the prescribing clinician; you may advise to stop pending medical guidance

Clinical vignette: wheezing and hypotension after taking an antibiotic—diagnosis and mechanism.

Type I anaphylactic reaction; IgE-mediated mast cell degranulation causing bronchospasm and vasodilation—medical emergency

Immediate chairside priority in suspected anaphylaxis.

Recognize airway/blood pressure risk; initiate emergency management and activate EMS; this is a life-threatening situation

Clinical vignette: severe dry mouth, dry eyes, many caries—category and action.

Misdirected (autoimmune) process consistent with Sjogren's; manage oral complications and refer for systemic evaluation

Clinical vignette: very itchy perioral reaction 2 days after exposure—type and treatment.

Type IV delayed hypersensitivity; symptomatic relief (e.g., topical corticosteroid) and avoid trigger; categorize as "too strong" hypersensitivity

Clinical vignette: new oral infection on tacrolimus after kidney transplant—interpretation.

Secondary immunodeficiency due to immunosuppression; heightened infection risk necessitating careful management and medical coordination

What are the main functions of antibodies?

Neutralization, agglutination, removal of antibody-antigen complexes, complement activation, helping NK cells, and activating monocytes/macrophages.

Do antibodies directly kill pathogens?

No, they do not kill anything directly; they primarily mark targets for destruction by other cells.

What is the FAB region of an antibody?

The fragment antigen-binding (FAB) region is where the antigen binding sites are located.

What is the FC region of an antibody?

The fragment crystallizable (FC) region is the "tail" or "bottom part" of the antibody.

Why is the FC region of an antibody important?

Many immune cells, such as mast cells, have Fc receptors that bind to this region, which can trigger cellular responses like histamine release.

What is the primary function of the variable regions on an antibody?

To allow the antibody to recognize and bind to a wide variety of different antigens.

What is the most abundant immunoglobulin in the body and the only one that can cross the placenta?

IgG

Which immunoglobulin is predominantly found on mucosal surfaces?

IgA

What is the structure of IgA when found in mucosal secretions?

It exists as a dimer (two units) held together by a J chain and a secretory component.

What is the origin of the secretory component of secretory IgA (sIgA)?

It is a piece of the Fc receptor from the epithelial cell that transports the IgA dimer across the mucosal barrier.

What is gingival crevicular fluid (GCF)?

It is a fluid found in the subgingival space (gingival crevice) that is more like a blood filtrate than saliva, containing proteins like albumin and predominantly IgG antibodies.

Which antibody is the first to be produced during a primary immune response?

IgM

A high level of IgM against a specific pathogen suggests what stage of infection?

The early stages of an infection.

Which antibody is primarily associated with allergic reactions and parasitic infections by binding to Fc receptors on mast cells?

IgE

What is the primary role of IgD?

It is primarily found as a B cell receptor on the surface of B cells and is not typically secreted as an antibody.

How are the vast number of different antibody specificities generated in the body?

Through random gene rearrangement during B cell development, creating a diverse repertoire of B cells before any antigen is encountered.

What are cytokines?

Small proteins that act as cellular messengers, secreted by immune cells and other cell types to regulate immune responses.

Which three pro-inflammatory cytokines are most important to know for oral inflammatory diseases like periodontitis?

IL-1, IL-6, and IL-8

What is the main function of IL-8?

It is a chemokine that attracts neutrophils to the site of inflammation and can be secreted by macrophages and epithelial cells.

Which cytokine is known for its anti-inflammatory properties, helping to downregulate the immune response?

IL-10

Which pro-inflammatory cytokine is a major player in the pathogenesis of inflammatory diseases like periodontitis and rheumatoid arthritis?

IL-17

What are interferons (IFNs)?

Cytokines that are crucial for antiviral defense; an infected cell releases them to warn neighboring cells to upregulate their antiviral mechanisms.

Which cytokine is primarily involved in wound healing?

Transforming growth factor-beta (TGF-beta)

What are the two main immune strategies in the oral cavity?

Immune exclusion and inflammation.

Define "immune exclusion" in the context of the oral cavity.

The process of inactivating and clumping antigens (like microbes) so they can be swallowed and eliminated from the body.

What are defensins?

Small antimicrobial peptides produced by epithelial cells and various immune cells that contribute to the innate defense in the oral cavity.

How does the oral epithelium act as a physical barrier?

Through keratinization, a basement membrane, and the constant shedding of its top layers (desquamation), which helps remove adherent bacteria.

How can some periodontal pathogens, like P. gingivalis, evade the immune system?

By hiding inside epithelial cells, where they are protected from antibodies.

What is "colonization resistance"?

The process where the normal oral microbiota prevents pathogens from establishing themselves by competing for space and nutrients and by producing antimicrobial substances.

What is the term for a healthy, stable microbial community, such as in the oral cavity?

Eubiosis

What is the term for a disturbed or imbalanced microbial community, which can lead to disease?

Dysbiosis

What often causes dysbiosis in the oral cavity, allowing opportunistic pathogens like Candida to thrive?

Disruption of the normal microbiota, often due to antibiotic therapy.

"Does periodontal disease follow Koch's postulates (one germ, one disease)?"

No, it is typically caused by dysbiosis—an imbalance in the entire bacterial community—rather than a single pathogen.

What are T helper 17 (Th17) cells?

A subset of T helper cells that are the main source of the pro-inflammatory cytokine IL-17 and play a major role in periodontitis.

In periodontal disease, IL-17 contributes to tissue destruction by affecting which cell types?

Epithelial cells, fibroblasts (soft tissue), osteoblasts, and osteoclasts (bone).

In a healthy state, what is the role of IL-17 in the oral epithelium?

It helps maintain the mucosal barrier by upregulating tight junction proteins and inducing the secretion of antimicrobial peptides.

What are the two main characteristics of adaptive immunity?

Specificity (lymphocytes recognize a specific antigen) and Memory (faster, stronger response on second exposure).

What type of molecule are most antigens?

Proteins, though they can also be lipids or carbohydrates.

How does a primary immune response differ from a secondary immune response?

The primary response is the first time the body sees an antigen; the secondary response is much higher, quicker, and the resulting antibodies/cells persist longer.

Why do vaccines work?

They create a primary immune response and generate memory cells, so if you are later exposed to the pathogen, you mount a rapid and robust secondary response.

What are the two main types of lymphocytes in the adaptive immune system?

B cells and T cells.

What is the general function of T cells?

They perform the cellular response and help with the B cell response.

What is the general function of B cells?

They differentiate into plasma cells, which then produce and secrete antibodies.

Why do lymph nodes swell during an infection?

Lymphocytes in the secondary lymphoid tissue recognize a pathogen, become activated, and proliferate (make many copies of themselves), causing the swelling.

What is the role of C-reactive protein (CRP)?

It is an acute phase protein often used as a clinical marker for inflammation.

What are the two main types of T cells?

Cytotoxic T cells and Helper T cells.

How can you differentiate between cytotoxic and helper T cells?

By their surface molecules: Cytotoxic T cells have CD8, and Helper T cells have CD4.

What does it mean for an antigen-presenting cell (APC) to "present" an antigen?

The APC modifies the antigen and displays it on its cell surface using an MHC molecule for a T cell to recognize.

What is the function of the T cell receptor (TCR)?

It recognizes the specific antigen (e.g., a piece of a virus) being presented by another cell.

What is the function of the CD8 molecule on a cytotoxic T cell?

It recognizes and binds to the MHC class I molecule, which helps solidify the interaction between the T cell and the target cell.

What is the function of the CD4 molecule on a helper T cell?

It recognizes and binds to the MHC class II molecule on an antigen-presenting cell.

What is the primary role of regulatory T cells (T-regs)?

" To ensure the immune system does not react against things it shouldn't (i.e., self-antigens)."