Section 1
Preview this deck
increase functioning of B cells
Front
| 5 | 0 | ||
| 4 | 0 | ||
| 3 | 0 | ||
| 2 | 0 | ||
| 1 | 0 |
Active users
2
All-time users
2
Favorites
0
Last updated
1 year ago
Date created
Mar 14, 2020
Cards (135)
Section 1
(50 cards)
increase functioning of B cells
t helper (cd4)
mature and differentiate in thymus have T- cell receptors (TCRs) on the cell surface to recognize Ags TCR is linked to a membrane protein of CD3 cell receptor= TCR-CD3 complex
t lymphocytes
antiviral properties
interferons (IFNs)
destroys fibroblasts
lymphotoxin (LT)
innate immune response found in microcirculation (not surrounding tissue) respond immediately without input/ chemical mediators responds to virus- infected and cancer cells IMPAIRED function in immune deficiency disorders
natural killer cells
B- memory cells: clone themselves and then function as APCs Plasma cells: produce specific antibodies
two types of B- lymphocytes
immune system may overreact to Ag
hypersensitivity
rapid, first line of defense against injury
inflammatory response
antibody- mediated immunity b cells are the primary cells protection against bacteria and viruses immediate response
humoral immunity
B- cell and T- cells produce lymphokines monocytes or macrophages produce monokines variety of functions (type specific): example- chemokines induce chemotaxis controlling infection
cytokines
educates the cells (T cells)
thymus
make up about 25% of WBC population mobile increased longevity round nucleus and less cytoplasm recognize and respond to receptor on Ag surface 3 types with different functions
lymphocytes
from stem cells in bone marrow, B cells mature in lymphoid tissue, and travel to site of injury when stimulated by an Ag
B- lymphocytes
filters RBCs
spleen
early immune response (like IgD) clumping of Ag proteins primary role most efficient Ig in activating compliment system largest of Igs
IgM
turn off functioning of B cells
t suppressor (cd8)
are signaling proteins produced by cells of the immune response role in activation of immune response aka immunomodulators: affect behavior of other cells, alter the immune response communicators
cytokines
various functions involving WBCs and fibroblasts
tumor necrosis factor
primary function to process antigenic material and present it to other cells of the immune system aka Ag presenting cell Function like the B cell and macrophage- messenger between innate and acquired immunity
dendritic cells
activates B lymphocytes found on B lymphocyte cell surfaces (no release into serum or body fluids)
IgD
during development in the blood, cells develop dendrites when activated, migrate to the lymph tissue interacting with T and B cells to initiate an acquired immune response in skin and mucosa (specialized dendritic cell) oral mucosa (langerhans cells)
dendritic cells
Ags are presented to T cells via B cells that have major __________________ complex (MHC) proteins on their surface aka human leukocytes antigens (HLAs) role in organ transplantation (success or failure)
histocompatibility
follows exposure to an antigen involves memory- remembers and responds quicker than inflammatory responses involves complex network of WBCs may result in tissue damage and disease as it fights
how does acquired immunity work
foreign substances the immune system uses to defend the body
antigens
initiates a immune response, process B cells, removes antigens
Lymphatic system
bone marrow, thymus, spleen, lymphatic vessels and nodes, Mucosa- associated lymphoid tissue (ex. oral-pharyngeal)
organs of immune system
immune system may recognize itself as antigen (Ag)
autoimmunity
stimulate WBC proliferation and other function
interleukins (ILs)
secreted by plasma cells in skin and mucous membrane seen in hypersensitivity or allergic reactions triggers release of histamine protects against parasitic infections
IgE
are antibodies (Ab) circulating in plasma produced by the B lymphocytes in response to a specific antigen (Ag) specific Ab combined with specific Ag= immune complex (IgG, IgM, IgA, IgE, IgD)
Immunoglobulins (Ig)
bone marrow turns into
immunity cells
75-80% of circulating Abs target viruses, bacteria, toxins ONLY Ig to cross the placenta, hence first passive immunity to newborns active in secondary immune response
IgG
detect and remove antigens
mucosa- associated lymph tissue
innate, acquired
immune system may be:
aka immunogens: chemicals, food proteins, products of microbes (LPS), abnormal tissue cells (tumor cells), donor cells, our own tissue cells (autoimmune diseases), microbes
examples of antigens
an increased responsiveness due to memory of an antigen
immunity
antibodies created by another person innate- mothers Ab (IgG) crosses placenta to protect developing fetus acquired- immediate protection; short lived; post- exposure prophylaxis
passive immunity (receives Ab)
cellular immunity t cells are the primary cells regulates both immune responses delayed response
cell mediated immunity
Attack virally infected cells or tumor cells
t cytotoxic (cd8)
Found in connective tissue during inflammation Accessory cell: in the inflammatory process (phagocytosis) and in the immune response (helping B- and T- cells by presenting Ags- an APC) No memory Amplifies the immune system
macrophages
the immune response to a specific antigen is much faster and stronger the ______________ time it enters the body
second
2nd line of defense; able to remember and respond quickly to antigens encountered a second time
immune response
stimulates macrophage emigration
macrophage chemotactic factor (MCF)
activates macrophages to produce and secrete lysosomal enzymes
macrophage- activating factor (MAF)
primary WBCs in immune response
lymphocytes
restores injured tissue from both responses
repair
Lymphocytes:B lymphocytes, T lymphocytes, Natural Killer cell macrophages dendrites
immune response cells
reduces proliferation of microorganisms in body fluids protects respiratory, GI and genitourinary tracts part of primary immune response serous (blood) secretory (saliva, tears, breast milk)
IgA
immune system may not recognize the Ag as foreign
immunodefficiency
inhibits macrophage activity
migration inhibitory factor (MIF)
Section 2
(50 cards)
autoimmune diseases (ex SLE)
type III (immune complex) hypersensitivity
connective tissue diseases manifest as type 2,3,4 hypersensitivity recognition mechanism breaks down and certain body cells no longer tolerated systemic or single organ genetic implications oral manifestations
autoimmune diseases
aka allergic reactions Ags called allergens haptens are exaggerated immune responses four types
hypersensitivity reactions
drugs may act as antigens multifactorial: route of administration (topical more than oral or parenteral), autoimmune disease, multiple allergies Type 1, 3 or 4 hypersensitivity
drug hypersensitivity
forms: reticular- wickhams striae (classic appearance), erosive or bullous, desquamative gingivitis lichenoid mucositis diagnosis: clinical, histologic,possible inc risk for squamous cell carcinoma (erosive form) treatment
lichen planus
granulomatous diseases (ex TB); Graft and organ transplant rejection
type IV (cell mediated) hypersensitivity
result of direct contact with allergen type 4 hypersensitivity contact mucositis: erythema, edema, itching, burning, vesicles, ulcers, anesthetic preservatives, topical meds, dental materials, flavoring (cinnamon oil) in toothpaste and gum erythema, edema, vesicles causes crusting, scaly lesion latex gloves and powder
contact mucositis and contact dermatitis
immunopathologic condition immune system fails to function due to decrease in #, function, and relationships of WBCs congenital or acquired oral manifestations
immunodeficiency
clinical appearance: erythema, ulceration, bullae, Nikolsky sign Diagnosis: biopsy/ histological (no degradation of basal cells; plasma cells and eosinophils in CT) tx: topical or systemic corticosteroids
mucous membrane pemphigoid
antibodies created by the person Innate-from exposure to disease acquired- immunization
active immunity (producing Ab)
2 categories: 1) single system (bone > skin, lymphnodes, lung) 2) Multi system (bone, skin, liver, spleen, bone marrow) Diagnosis: biopsy and histological definitive diagnosis in Birbeck granule found in cytoplasm of dendritic cell treatment: excision, radiation, chemo
langerhans cell histiocytosis
severe and progressive, most common of 3 forms skin and mucous membranes affected cause intra- epithelial blister (acantholysis) majority > 50 years clinical appearance: (1st sign seen orally in 50% of cases): ulcers, vesicles, bullae, bullae --->Nikolsky sign Histologic findings: Tzanck cells
pemphigus vulgaris
rare genetic or developmental involve B-cells, T- cells, or both Examples: isolated IgA deficiency, X-linked congenital agammaglobulinemia (bruton disease), thymic hypoplasia (digeorge syndrome), severe combined immunodeficiency, leukocyte adhesion deficiency
primary immunodeficiencies
diagnosis: multi- organ involvement, antinuclear Abs (ANAs) in serum treatment and prognosis: dependent upon degree of disease activity, extremely complex, requires MD complex
systemic lupus erythematosus
acute and chronic, a syndrome etiology unknown cell mediated and humoral immunity affected females 8x > males; african americans 3x skin lesions most common symptom: butterfly rash erythematous lesions on finger tips oral lesions- erythematous plaques, erosion, lichen planus- like
systemic lupus erythematosus
occurs immediately aka anaphylactic hypersensitivity IgE from plasma cells, renders histamine release, causing increased vascular dilation, permeability causes edema and constriction of smooth muscle in the lung ex- hay fever, hives, asthma, anaphylaxis due to bee stings, latex, peanuts, penicillin, mold
type 1 hypersensitivity
immune system cells are produced in which of the following organ systems
bone marrow
skin and oral mucosa hypersensitivity reaction caused by inc permeability in superficial CT due to histamine release from mast cells stimulated by IgE and activation of IgG or IgM Diagnosis- clinical appearance and history uticaria (hives)- localized erythema and edema, itching angiodema- diffuse edema; due to inc vascular permeability in deep CT
uticaria and angiodema
arthritis and arthralgia, raynaud phenomenon, myalgia and myositis, retinal vasculitis, psychoses and depression, seizures, cardiac, kidney disease, thrombocytopenia
syndrome
aka cicatricial pemphigoid and benign mucous membrane pemphigoid chronic 2x more common in women, > 50 years tissues affected: oral mucosa, gingiva- most common (desquamative gingivitis), conjunctiva, genital mucosa, skin
mucous membrane pemphigoid
diagnosis: biopsy/ microscopy/ lab tx and prognosis: corticosteroids (mortality rate of 8 - 10% in 5 years is related to complications of corticosteroid tx
pemphigus vulgaris
aka Sutton disease > 1 cm deep and last longer than minor aphthous ulcers very painful posterior of the mouth association with HIV, Behcet syndrome, Crohns, Reactive arthritis
major aphthous ulcers
benign and chronic unknown etiology rare middle age most common skin and/or oral mucosa, symmetrical lacelike pattern small, papular, domed white nodule buccal mucosa > tongue, lips, floor of mouth, gingiva
lichen planus
aka langerhans cell disease rare characterized by histiocyte- like cells (LC) and eosinophils known to be myeloid dendritic cells 50% of cases < 15 years of age single bone lesions most common 10-20% in jaw etiology (unclear): reactive, neoplastic, primary immunodeficiency
langerhans cell histiocytosis
occurs immediately aka cytotoxic hypersensitivity- Ab combines with an Ag bound to the surface of tissue cells, usually a circulating red blood cell (RBC) IgG and IgM activate compliment system- this destroys the tissue that has that Ags on the surface of its cells (eg Rh incompatibility)
type 2 hypersensitivity
the humoral response involves the production of
antibodies
the study of immune reactions involved in disease; the study of diseases caused by the malfunctioning of the immune system
immunopathology
hay fever, asthma, skin reactions, anaphylaxis
type I (anaphylactic) hypersensitivity
> 70 years of age oral lesions less common; gingival lesions similar to mucous membane pemphigoid Diagnosis: biopsy/ histological and circulating autoAbs Tx and Prognosis: NSAIDs or systemic corticosteroids
bullous pemphigoid
sjogren syndrome, systemic lupus erythematosus, pemphigus vulgaris, mucous membrane pemphigoid, bullous pemphigoid, behcet syndrome
autoimmune diseases in oral cavity
apthous ulcers, urticaria and angiodema, contact mucositis, fixed drug eruptions, erythema multiforme, lichen planus, reactive arthritis, langherhans cell disease
oral diseases w/ immunologic pathogenesis
affects minor and major salivary glands bilateral parotid gland enlargement occurs in about 50% of patients oral discomfort caused by dry mouth, erythematous lips cracked and dry loss of filiform and fungiform papillae on the dorsum of the tongue, dysgeusia high risk for caries, perio disease and oral candidiasis
sjoegren syndrome
xerostomia, xeropthalmia, Raynaud phenomenon diagnosis (based on 2 of 3) 1) keratoconjunctivitis sicca 2) xerostomia 3)Rheumatoid arthritis or another autoimmune disease lab abnormalities- rheumatoid factor & autoAbs etc
sjoegren syndrome
autoimmune hemolytic anemia
type II (cytotoxic) hypersensitivity
acute unknown etiology (hypersensitivity, antibiotic, analgesics, mycoplasma pneumoniae) young adults < 30 years major and minor forms prodromal symptoms diagnosis: exclusion of other diseases and clinical appearance: target or bull's eye lesion macules, plaques, bullae oral lesions (lateral tongue) and/or skin lesions
erythema multiforme
chronic, recurrent,rare inflammation of blood vessels clinical finding: oral ulcers (painful, recurrent aphthous); postular lesion at injection site/ genital ulcers/ ocular inflammation/ skin lesions (pustular lesion) 30-40 years of age gender predilection varies between countries diagnosis: 2 of 3 manifestations, pathergy test Tx and prognosis: corticosteroids and immuno
behcet syndrome
delayed hypersensitivity aka cell-mediated immune response T- cells sensitized to a particular Ag initiate an inflammatory response resulting in cell damage/ death examples: contact dermatitis- poison ivy, nickel, etc graft or organ rejection
type 4 hypersensitivity
caused by an underlying disorder more common than primary result of immunosuppressive drug use disorders with accompanying immunodeficiency: malnutrition, renal diseases, HIV, diabetes
secondary immunodeficiencies
Triad( aka Reiter syndrome) 1) arthritis 2) urethritis 3) conjunctivitis genetic influence (HLA- B27 antigenic marker) 1-6 weeks post STD or GI infection males> females oral lesions: aphthous- like ulcers and geographic- like tongue
reactive arthritis
hypersensitivity reactions immune deficiency diseases autoimmune diseases
3 categories of immunopathology
cell mediated response (inc lymphocytes) common oral finding- professional students painful, etiology unclear: trauma, iron/folic acid/ B12 deficiencies, stress, genetic predisposition, systemic disease association 3 forms
aphtous ulcers
langerhans cell histiocytosis older children and young adults skull and mandible looks like perio or periapical inflammation treatment- surgical excision/ radiation
eosinophilic granuloma of bone
least common form 1-2 mm resemble herpes simplex ulcers painful, occur in groups
herpetiform aphthous ulcers
cell mediated (T- cell) or humoral (B-cell) response primary (genetic) or secondary infection most common complication, dependent on type of immunodeficiency
immunodeficiencies
type 3 hypersensitivity reaction immune complexes are deposited along the endothelial walls of blood vessels inflammation causes vasculitis with damage to the vessel wall creates erythema and edema in superficial layers of the skin or mucosa barbituates, chlorhexidine, lidocaine, sulfonamides, tetracycline, penicillin fixed location latent period prior to appearing clinical appearance: single or multiple patches or macules/ erythema, edema, pain and itching/ skin or rarely, mucous membranes
fixed drug eruptions
the immune system defends the body against foreign substances called
immunogens
occurs immediately aka immune complex hypersensitivity IgM, IgA, IgG form Ag/Ab complexes with circulating microorganisms in the blood complexes are deposited in various body tissues phagocytosis by neutrophils causes local or systemic tissue destruction rheumatoid arthritis lupus erythematous
type 3 hypersensitivity
most common form discrete, round or oval ulcers lining mucos 1 cm or smaller erythematous halo surrounding a yellowish- white fibrin surface anterior> posterior prodromal period of of 1 to 2 days
minor aphthous ulcers
affects salivary glands and lacrimal ducts (aka sicca syndrome) females > males cellular and humoral immunity involved primary vs secondary sjogren - 50% have a 2nd autoimmune (secondary sjoegren)
sjoegren syndrome
formerly a severe form of erythema multiforme a variant of toxic epidermal necrolysis (YEN): adverse reaction to certain drugs/rare/ older adults/ females> males treatment prognosis
stevens johnson syndrome
Section 3
(35 cards)