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Microbio Final Exam > Chapter 18: Autoimmune Disorders > Flashcards

Chapter 18: Autoimmune Disorders Flashcards

1
Q

How do autoimmune disorders occur?

A

Can happen when out T and B cells that targeted our own cells failed to delete during development stayed

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2
Q

Molecular mimicry with Strep Pyogenes

A

Mimics the proteins on our heart and our antibodies formed against strep pyogenes can end up targeting our heart

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3
Q

Which cell turns off immune response when no longer needed?

A

T Regulatory cells

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4
Q

What can cause an autoimmune disease as you grow older?

A

You can acquire a change in your cell makeup, possibly in A.A and your immune system picks up the mutation change as foreign and has an immune response

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5
Q

What is an autoimmune response?

A

Mounting an immune response to your own tissue

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6
Q

Treatment of autoimmune diseases

A

No treatment to cure but you can take immune suppressor drugs

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7
Q

Autoantibodies

A

Antibodies against ones own tissue (a) can be T cell mediated as well (b) cell destruction in various hypersensitive reactions

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8
Q

Auto-immunization

A

(1) The process by which hypersensitivity to “self” develops (2) Response usually sustained and long-lasting and can cause long-term tissue damage

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9
Q

Mechanism of autoimmunity: Genetic factors

A

these factors may predispose a person toward autoimmune disorders likely to develop autoantibodies to the same or to a different single organ

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10
Q

Mechanisms of autoimmunity: Antigenic or molecular mimicry

A

(1) Th cells might attack tissue antigens that are similar to antigens of some pathogens (2) Rheumatic fever can lead to rheumatic heart disease later in life because heart valve tissue is seen similar to certain streptococcal antigens

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11
Q

Mechanisms of autoimmunity: Thymus and development of Th cells

A

TH cells instead of just recognizing foreign antigens recognize self-antigens (happens if the clonal deletion doesn’t take out the self-reactive TH cells)

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12
Q

Mechanisms of autoimmunity: Mutations

A

Might give rise to aberrant proteins to which B cells react, producing plasma cells that make autoantibodies

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13
Q

Mechanisms of autoimmunity: Viral components

A

(1) Inserted into host cell membrane (2) might act as antigens or virus antibody complexes (3) Might be deposited into tissue

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14
Q

Mechanisms of autoimmunity: Sympathetic nervous system and parasympathetic system

A

When NS is damaged, the number of regulatory T cells decreases

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15
Q

Autoimmune disease: Myasthenia Gravis

A

(1) Affects women early on, men later on (2) Affects skeletal muscles of the limbs and those involved in eye movements, speech and swallowing (affects single organs) (3) Progressive weakness of muscle fatigue (4) Eyelid drooping (5) Muscle contraction is prevented by IgG which block Acetylcholine receptors or cause reduction in number of receptors (6) People tend to have tumors of the thymus as a result

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16
Q

Autoimmune disease: Rheumatoid Arthritis

A

(1) Affects mainly the joints of the hands and feet (2) Initially a T cell problem (3) Joints are affected in pairs, meaning on both sides of the body (4) Inflammation and destruction of the cartilage in joints

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17
Q

Rheumatoid Arthritis: cell action

A

(1) People with RA have a Th2 cell dependent B cell response to the Fc portion of IgG (2) IgG complex leads to RA

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18
Q

Rheumatoid factors

A

Autoantibodies used in diagnostic test of RA

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19
Q

Hydrocortisone and Aspirin

A

Can be used to ease pain and inflammation

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20
Q

Systemic Lupus Erythematosus

A

(1) SLE is a systemic autoimmune disease derived from reddened skin rash (erythematose) that resembles a wolfs mask (lupus) (2) Autoantibodies IgA, IgM, IgG are made against components of DNA and blood cells, neurons and other tissue (3) Immune complexes deposited between dermis and epidermis, joints, blood vessels leads to inflammation (4) Butterfly shape rash (5) No cure (Rash precipitated through exposure to sunlight

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21
Q

Transplantation

A

Transfer of tissue called “graft tissue” from one site to another

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22
Q

Autograph

A

Involves graphing of tissue from one part of your body to another

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23
Q

Isograft

A

Skin graft between genetically identical individuals

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24
Q

Allograft

A

Graft between 2 people who are NOT genetically identical

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25
Q

Xenograft

A

A transplant between individuals of different animal species

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26
Q

Transplant rejection

A

Rejection of skin tissue due to destruction of the grafter tissue by the recipients immune system (Depends on T cells)

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27
Q

Graft Versus Host Disease (GVS)

A

Less common, transplanted tissue contains immunocompetent T cells that launch a cell mediated response against the recipients tissue (commonly in immunodeficient individuals receiving bone marrow transplant and cannot reject the graft tissue

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28
Q

Histocompatibility antigens

A

All human cells and those of other vertebrate that have a set of self-antigens

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29
Q

MHC

A

Genes that produce histocompatibility antigens

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30
Q

Who can have identical MHC molecules

A

Twins

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31
Q

Importance of matching Histocompatibility complex

A

Histocompatibility antigens need to be the same in order for tissue to be accepted, because if not, T cells destroy donor tissue

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32
Q

HLAs (Human Leukocyte antigen)

A

determined by a set of genes located on chromosome 6

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33
Q

HLA- B

A

Highly variable

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34
Q

HLA-DR

A

antigens are known to generate the strongest rejection reactions

35
Q

Presence of HLA antigen is associated with higher than normal risk for developing what?

A

Specific diseases

36
Q

Transplant rejection

A

Displays specificity and memory and is associated with mismatched HLA-DR antigens (found on T cells and macrophages responsible for rejection)

37
Q

Which T cells are the ones most likely to reject tissue?

A

TH2 cells (they also stimulate cytotoxic T cells which reject the transplant through cell mediated cytotoxicity

38
Q

TH2 cells also activate B cells to produce what during transplant rejection?

A

Produce plasma cells and antibodies that cause rejection through lytic damage

39
Q

Macrophages that are activated by TH1 cells do what during transplant rejection?

A

Secrete inflammatory mediator and cause cytotoxic damage to transplant

40
Q

NK cells actions during transplant rejection

A

Finds MHCII protein that are different than tissue of person and immediately start to take charge and release perforin

41
Q

TH1 role in transplant rejection

A

Th1 cells activate macrophages which produce an inflammatory mediators

42
Q

Th2 role in transplant rejection

A

Th2 cells trigger both Tc and B cell activation and B cells then give rise to plasma cells that synthesize antibodies (including HLA-DR) and with complement, rejects transplant. Tc cells just activate cell mediated toxicity and them reject transplant.

43
Q

Ways to minimize rejection

A

Tissue typing and immune suppressant drugs

44
Q

Hyper acute rejection

A

A cytotoxic hypersensitivity reaction occurs when the recipient is already sensitized at the time the graft is done leading to extensive damage right away

45
Q

Accelerates rejection

A

Takes several days because it requires cells to reach the graft

46
Q

Acute rejection

A

Occurs in days to weeks requiring T cell sensitization after transplantation

47
Q

Chronic rejection

A

Begins months to years after transplantation, slow process typical of kidney and cardiac transplants

48
Q

Reasons as to why mothers can tolerate fetus

A

(1) Considered “immunologically privileged site” (2) Cells on the surface and interior of the fetal portion of the placenta do not express MHC molecules (3) Certain HLA molecules prevent maternal NK cells from killing fetal cells

49
Q

Alpha-fetoprotein

A

Protein produced by fetus has immunosuppressant properties

50
Q

Women who have similar or different tissue types with their husbands suffer more miscarriages?

A

Similar

51
Q

Foreignness of the sperm may trigger what?

A

Triggers maternal production of blocking antibodies that protect the fetus

52
Q

Immunosuppression

A

(1) minimizing of immune reactions (2) Specifically leads to immune systems ability to tolerate only the antigen in [ex: transplants tissue] and allows the immune system to continue to respond to other infectious agents

53
Q

Radiation or cytotoxic drugs

A

Impairs the immune response and minimizes rejection reactions (radiation destroys lymphocytes which inhibits the immune systems ability to recognize infectious microbes)

54
Q

Cytotoxic drugs

A

Damage cells, Prevents B and T cell division

55
Q

Drug reaction

A

Considered a hapten because it needs to bind to a protein in the body to be recognized

56
Q

Drug molecules

A

Usually too small to act as allergen

57
Q

Drug combined with proteins can induce what?

A

Hypersensitivity

58
Q

Type 1 hypersensitivity

A

Can be caused by various drugs, mostly localized anaphylactic reactions, usually occurs with injection

59
Q

Type 2 hypersensitivity

A

A drug may bind directly to the plasma membrane of a blood cell, when drug binds to drug plasma protein, complex binds to membrane of blood triggering autoantibody production through compliment

60
Q

Type 3 Hypersensitivity

A

Appears as serum sickness and can be caused by any drug that participates in the formation of immune complexes, symptoms appear several days after

61
Q

Type 4 hypersensitivity

A

Occurs as contact dermatitis after topical application of drugs

62
Q

Immunodeficiency diseases are due to what?

A

Adsence or deficiency of active lymphocytes, NK cells or phagocytes

63
Q

Primary immunodeficiency diseases

A

Caused by genetic defects in embryological development such as failure of the thymus gland or peyers patches to develop normally

64
Q

Result of primary immunodeficiency

A

Lack of T cells or B cells or defective B and T

65
Q

Agammaglobulinemia

A

B cell deficiency

66
Q

DiGeorge syndrome

A

Results from a deficiency of T cells caused by an agent that interferes with embryological development of the thymus gland

67
Q

SCID (Severe combined immunodeficiency)

A

Debilitating because both B and T cells are absent

68
Q

Gene Therapy

A

Attempts to replace defective gene with a functional therapeutic copy of that gene

69
Q

Serology

A

Antibodies in serum of blood, try to find titer of specific antibodies

70
Q

Titer

A

Concentration of antibody in serum

71
Q

Secondary Immunodeficiency diseases

A

Not genetic, can be impacted by physical condition and stress

72
Q

3 things that can cause secondary immunodeficiency diseases

A

(1) Infectious agents: TB,AIDs, HIV, measles, leprosy (2) Malignancies: Hodgkins disease or multiple myeloma (3) Immunosuppressants: chemotherapeutic drugs, antibiotics, radiation

73
Q

Precipitin Test

A

Done to see if someone has antibodies to a specific virus (done in liquid)

74
Q

Zone of equivalence

A

Equal amount of antigens and antibodies present, Agglutination

75
Q

Zone of excess antigen

A

You see a complex form , free antigens floating

76
Q

Zone od excess antibody

A

Antibodies are more present than soluble antigen

77
Q

What happens when IgG or IgM react with soluble antigens?

A

They form complexes

78
Q

Immunodiffusion test

A

Done in agar, poke holes in agar and put antibody on the outside of each hole and then antigen goes inside the agar hole (if they recognize each other, there will be a line of spreading)

79
Q

Blood Typing

A

RBCs and Anti Rh antibodies cannot be seen with naked eye when bound together, SO Rabbit anti-human immunoglobins are added for an agglutinated RBC that can be seen with the naked eye

80
Q

Complement fixation assay: Negative

A

(1) Negative is person does not have antibodies to virus protein (2) Complement added and was not fixed/attached meaning no antibody-antigen complex (3) There was no antibody for antigen in humans serum (4) Loads of complement are free and lysing RBCs because aren’t bound to a complex

81
Q

Complement fixation assay: Positive

A

(1) Positive test person has antibodies to virus (2) you start with a complex (3) Complement is added (4) Compliment binds with antibody-antigen complex (5) Add indicator RBCs to have better viewing (6) RBCs don’t lyse because complement is tied up with persons antibody-antigen complex

82
Q

Immunofluorescence

A

Fluorescence dye put on part of the constant part of the antibody so that under UV microscope the dye on the antibodies fluoresce

83
Q

ELISA

A

(1) Enzyme linked Immunosorbent Assay (2) done with radioactive molecules (3) uses enzyme linked dyes (4) Enzyme clips colorless substrate that is added, forming a red product due to complex formed (5) In hospitals for faster results, there is a red dye on the strip rather than it being enzyme linked

Microbio Final Exam (11 decks)

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