Exam 1 The Immune System Flashcards by Jessica Lahrs

What is included in the innate immune system?

1) Epithelial barriers of the skin, gastrointestinal and respiratory tracts
2) Phagocytic cells (neutrophils and macrophages
3) NK cells
4) Acute phase proteins (complement, c-reactive protein)

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What is included in adaptive immunity?

1) Humoral: B cells, plasma cell, antibodies
- important for fighting agents in the blood, mucosal secretions, and tissues
2) Cell-mediated: work by directly killing infected cells and activating phagocytes to kill the offending agent
- important in reacting to intracellular agents–>tumors, parasites

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What are the two hallmarks of the adaptive i/s?

specificity

- memory

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Do macrophages recognize bacteria yeast and fungi as different?

No–just knows its not self

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What are specific killers?

Its and T cells

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What is the culmination of innate and adaptive immune system?

inflammation

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How many antigens does a T cell receptor see?

one–each t cell receptor on an individual cell has the same specificity

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What cell has CD4+?

Helper t cells

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What cell has CD8+?

Cytotoxic t cells

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What is the ultimate boss of the immune system?

Helper t cells

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What T helper cell:

Releases: IL-2, IFN-y
Causes cell mediated responses: neutrophils, macrophages, and some CD8+ t cells to kill things

TH1

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What binds MHC class II?

CD4+

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What binds MHC Class I?

CD8+

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What is the job of CD8+ cells?

their job is to kill things in association with MHC class I

intracellular parasites
viruses

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What is CD3+ used for?

part of TCR complex important in cell signaling

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Do B cells secrete antibodies?

no-PLASMA cells

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What is the surface ig? (sIg)

it is on B cells and is a receptor for antigen

- when a B cell gets help from a CD4+ t cell it becomes a plasma cell

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What secretes antibodies and then dies?

Plasma cells

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How many subclasses does IgG have?

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How many subclasses does IgA have?

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What are the major isotypes of Igs?

IgG, IgM, IgA, IgD, IgE

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What cell has these functions:

1) Process and present antigen as they have MHC class II
- internalize foreign materials, breaks them into pieces, and then puts them on the cell surface in association with MHC class II
2) Release cytokines like IL-12, which is important for activating neutrophils and other macrophages
3) immune surveillance of bacteria and tumors is a major function of this cell

Macrophages

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What is the job of dendritic cells (nodes) and langerhans (skin) cells?

1) Their job is to present antigen through both MHC Class I and MHC class II
- class I and class II are found at high levels on the cell surfaces of this unique cell type
- poorly phagocytic, but they pinocytose everything in their surroundings

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What is the job of dendritic cells (nodes) and langerhans (skin) cells?

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Explain NK cells

``` Definition and morphology: -large granular lymphocytes (LGLS) -granules contains enzymes Function: lyse (break open)- 1) tumor cells 2) virally infected cells ```

Most cytokines are?

paracine-on adjacent cell

few cytokines are?

endocrine-at a distant site from the cell that produced the cytokine -IL-1

what are pleiotropic?

Interleukins affect MANY cell types, | EX: IL-1 stimulates fever but also activates T cells and macrophages

what are redundant?

different interleukins have the same effects - EX: IL-4 causes the production of IgE, but so does IL-13 - gives us a back up plan

Where do out MHC genes come from?

mom and dad - why you can't mix them during transplant - make same proteins

Genes of the MHC complex or HLA that start D

``` MHC CLASS II everything else is class I ```

What is the function of MHC?

- polymorphism: many types of the same molecules | - to present antigen in the form of peptides to TCRs on t cells

Does MHC present self or non self?

BOTH DUH | -MHC don't give a shit. Just presents whatever it has inside and show it to TCR to see if they care

How are the MHC molecules expressed from parents?

Co-dominantly - expressed equally, and you get one from both parents - this means that you have two of every MHC molecules, but 100s of them on the cell surface

Explain Haplotype

- linked MHC genes - this is what makes you from the immunological standpoint - used for determining: transplantation, DNA typing, etc

What is distributed on all nucleated cells of the body?

``` MHC class I MHC Class 1 = single polypeptide change ```

Where is MHC Class II molecules distributed? | MHC Class II = 2 poly peptide chain

-APCS; macrophages, dendritic cells, Langerhans cells and B cells

``` Type of hypersensitivity: -Anaphylactic or immediate -sequence of events: A) Sensitization by allergen 1) No i/r 2) Activation of Th2 cells (Ig production) 3) Secretion of IL-4 and IL-13 4) Plasma cell secrete IgE 5) Arms Mast cells ``` B) Pre-sensitized Mast cells 1) cross-linking of sIg- causes Ca influx, signals degranulation and release of many different mediators of inflammation C) Other factors: heparin affects complement activation

Type 1

Hypersensitivity means?

it attacks you

What are clinical manifestations of Type I?

A) Intake of protein antigens or drugs into: skin, food allergens and pollens B) within minutes urticaria, itching, erythema (hives) C) can lead to anaphylaxis, shock and even death

What type of hypersensitivity activated Th2 and secretes IL-4 and IL-13

Type 1

What type of hypersensitivity is antibody dependent? - IgM or IgG antibodies are directed at the cell or tissue that is directly responsible for tissue damage or altered function: 1) opsonization and and phagocytosis 2) complement-mediated and Fc receptor mediated inflammation - -transfusion reactions - -Rh incompatibility - -autoantibodies 3) Antibody mediated cellular dysfunction - -can create Ig to your own receptors like Graves disease

Type II

What hypersensitivity type is the Ig specific for the cell type?

Type II

What is the same between Type II and type III?

Complement, Ig, and neutrophils | -only difference is how its initiated

What type of Hypersensitivity is immune complex mediated? 1) Systemic immune complex -Formation in the circulation; overload of the phagocytic system so the complexes continue to circulate -Deposition of immune complexes-increase in vascular permeability due to cytokine release Favored sites: kidneys, joints, skin, heart and small vessels (BUT NOT SPECIFIC FOR THESE CELLS) -Inflammatory response initiated --Fever, urticaria, artsralgias, lymph node enlargement, proteinuria --C3a and C5a are complement components that recruit neutrophils and macrophages into the site

Type 3

What type of hypersensitivy that is cell mediated? 1) T cell mediated - CD4+ t cells, predominantly Th1 cells 2) Cellular cytotoxicity - in some cases CD8+ t cells are recruited to kill things but primarily CD4+ t cells activated the response 3) Granulomas--walling off - -persistent antigens, TB, parasites, fungi (fungi are almost always this type) - -macrophage wall of the organism and turn into fibroblasts to for the granuloma (granulomas are almost always this type)

Type 4

Type of Transplant rejection: 1) Hyper acute rejection occurs within a few hours - performed anti-donor antibodies - -sources are transfusions and multiple pregnant individuals 2) Concurrent with T cell mediated damage

Antibody-mediated rejection

Type of Transplant rejection: 10-14 days -Pre-sensitized CD4+ T cells direct CD8+ t cells, neutrophils and macrophages to attack and kill

T cell mediated rejection (acute)

Type of Transplant rejection: 1) occurs first months after transplantation 2) histologically there is extensive (non presensitized) CD4+ and CD8+ infiltration with mild edema and mild interstitial hemorrhage

Acute cellular rejection

Type of Transplant rejection: 1) rejection vasculitis 2) caused by antibodies and t cells of vasculature 3) histologic lesions may take the form of necrotizing vasculitis with endothelial cell necrosis, neutrophil infiltration, deposition of antibody, complement, fibrin and thrombosis

Acute vascular rejection

Type of Transplant rejection: 1) presents clinically late after transplantation (months to years) 2) the vascular lesions are caused by cytokines released by activated t cells that act on the cells of the vascular wall 3) does not respond to standard immunosuppression regimens

Chronic rejection

What are some methods of increasing graft survival?

1) matching at MHC class II-->because these are the T helper cells that tell everyone what to do 2) immunosuppression is used to manage rejection, but can result in tumors - -drugs--cyclosporin A and FK506 target CD4+ T cells (turning off CD4+ t cells) - -antibodies like anti-CD3 do not allow the T cell to trigger a response

What are some complications associated with the transplantation of other solid organs (i.e. kidneys, livers, heart, lung, pancreas) Should matching be done?

1) Host versus Graft disease (HVGD) - -host must be immune competent - -graft must be immune incompetent 2) there is not usually time

What are some complications associated with the transplantation of allogeneic hematopoietic cells? (i.e. aplastic anemia, leukemia) Should matching be done?

1) Graft versus Host disease (GVHD) - -host must be immune incompetent - graft must be immune competent--because the graft could kill the host and attack every cell in the body 2) absolutely

What is the purpose of self tolerance--clonal deletion?

kill off all the T cells that recognize self | -central tolerance

What is the purpose of clonal anergy?

Peripheral tolerance - T cells need a 2nd signal to be activated - B7 on the APC needs to bind to CD28 on the T cell - if no second signal then the T cell dies by apoptosis

What are the mechanisms of autoimmune disease?

1) loss of self tolerance - inheritance of susceptibility genes - environmental triggers (inflammation or inflammatory stimuli (bacteria)) - activation of self-reactive lymphocytes - tissue injury * autoimmune diseases basically occurs because break self tolerance and attack self

What type of hypersensitivity is malar skin rash? - DNA Igs get deposited at face (Ig doesn't bind to cell to kill cell) - symmetrical, raised, red rash on cheeks and nose called a butterfly rash - related to sun exposure

Type 3

What type of hypersensitivity is SLE? - kidney involvement is very important and most common cause of death in SLE patients 1) Mesangial Lupus Nephritis - -immune complexes deposit in the mesangium

Type 3

What type of hypersensitivity is RA -a systemic chronic inflammatory disease, primarily affecting the joints -1 of every 100 people affected, usually in the 4th and 5th decade of life Clinical manifestations: symmetric, polyarticular (many joints) arthritis -thought to be initiated by CD4+ t cells (activate macrophages and b cells)

Type 3

What syndrome occurs in women between the ages of 35 and 45 years of age -presents with dry mouth, lack of tears, complications associated with a lack of lubrication in these areas

Sjogren's syndrome

What uses CREST as a diagnosis | -can involve multiple organs, but primarily skin

Systemic sclerosis

What is the type of hypersensitivity where Plasma cells start producing Igs against your thyroid cell and thus block your TSH receptors? Basically Igs attacking our own cells

Type 2 | Graves disease

What is the type of hypersensitivity where you have antibodies blocking your Ach receptors so you have muscle weakness?

Type 2 | Myasthenia gravis

What type of hypersensitivity occurs when our Ig binds with an antigen and lodges somewhere? Where ever it lands it will stick and and then stimulate complement - this causes neutrophils to combine and MAC - localized destruction where ever this complex lands

Type 3

What type of hypersensitivity occurs when there are no Igs and it is cell mediated? -You have your tissue antigen then the helper T cells respond and kill that cell or activate macrophages to kill cell

Type 4 also know as delayed type (1-3 days later)

What is an Amyloid?

disorder of tissue folding - not a structurally homogenous protein - deposit in tissues - associated with alzheimers