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3s2: Infection and Immunity > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What are ways the immune system can go wrong?

A

Mutation / or error in key molecule/process/cell/organ that prevents normal function (Eg CGD, DiGeorge’s syndrome)
too many of a particular cell type (‘cytosis’) eg infectious
mononucleosis, or too few (‘penia’)
immunodeficiency versus hypersensitivity

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2
Q

What is haematopoiesis?

A

The formation of blood cellular components – occurs during embryonic development and throughout adulthood to produce and replenish the blood system
How most immune cells are produced

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3
Q

What are the normal functions of neutrophils and macrophages?

A

Chemotaxis, phagocytosis, killing and digestion

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4
Q

What are defects that can occurs at the different neutrophils and macrophage functions?

A

‘lazy leucocyte’ syndrome
hypogammaglobulinaemia
chronic granulomatous disease (CGD)
leukocyte adhesion deficiency (LAD)

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5
Q

What are benign disorders for neutrophils and macrophages?

A

Pelger-Huët anomaly
May-Hegglin anomaly
Chédiak-Higashi syndrome

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6
Q

What is the immune function of reactive oxygen species?

A

Reactive oxygen species generated in phagolysosome by NADPH oxidase
NO produced in cytoplasm by inducible nitric oxide synthase (iNOS), then diffuses into phagosome
Intermediates produced => effects

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7
Q

What is an overview of NADPH oxidase?

A

Multi-component enzyme that pre-exists in neutrophils and activated by signals from phagocytic receptors

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8
Q

What do macrophages for reactive species production?

A

Macrophages need IFN-gamma (cytokine) stimulation

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9
Q

What is an overview of CHRONIC GRANULOMATOUS
DISEASE?

A

Defect in component (gp91) of NADPH oxidase (X-linked) so dont produce ROS
Trouble clearing e.g. Staphylococcus aureus, Burkholderia cepacia, Aspergillus
Granulomas (tiny cluster of white blood cells and pathogens) form

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10
Q

What is an overview of NEUTROPHIL LEUCOCYTOSIS?

A

normal: 2.5-7.5x10^9/L
↑ in circulating neutrophils >7.5x10^9 /L frequent observed blood count change
Sometimes accompanied by fever

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11
Q

What can cause NEUTROPHIL LEUCOCYTOSIS?

A

Bacterial infections
Metabolic disorders (e.g lymphoma, acidosis, gout)
Acute haemorrhage or haemolysis
Drugs (e.g. corticosteroid therapy)

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12
Q

What is the problem with neutrophil leucocytosis?

A

Through production of toxic metabolites can cause organ damage

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13
Q

What is neutropenia?

A

Lower limit normal = 2.5x10^9/L (1.5x10^9/L for black and middle east people)

< 0.5x10^9/L
* recurrent infections

< 0.2x10^9/L
* congenital - Kostmann’s syndrome
* acquired (drug induced)
* e.g. anti-inflammatory, antibacterial, anticonvulsants, antithyroids,
hypoglycaemics

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14
Q

What is an overview of neutropenia?

A

benign
Cyclical
Immune
Auto, SLE, hypersensitivity
Infections
Part of general pancytopenia

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15
Q

What are HISTIOCYTIC DISORDERS?

A

histiocyte = tissue macrophage
Dendritic cell-related
Langerhans’ cell histiocytosis
Clonal proliferation of CD1a-positive cells
Single organ or multisystem
Latter affects children in 1st three years of life

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16
Q

How can HISTIOCYTIC DISORDERS be linked to macrophages?

A

Haemophagocytic lymphohistiocytosis
Rare, recessively inherited, or more frequently acquired
Increased numbers of histiocytes in bone marrow that ingest red cells, white cells and platelets

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17
Q

What is an overview of BASOPHIL LEUCOCYTOSIS
(basophilia)?

A

↑ above 0.1x10^9/L is uncommon
Myeloproliferative disorder (e.g. CML) usual cause

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18
Q

What is an overview of monocytosis?

A

↑ above 0.8x10^9/L is infrequent

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19
Q

What can cause monocytosis?

A

Chronic bacterial infections (tuberculosis)
Connective tissue disorders (SLE)
Protozoan infections
Hodgkin’s disease, AML and other malignanices myelodysplasia
Treatment with GM-CSF or M-CSF

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20
Q

What is an overview of infectious mononucleosis?

A

= EBV (Epstein-Barr virus) infection
Common cause of glandular fever (fever, sore throat,
lymphadenopathy and atypical lymphocytes in blood)
(other causes = cytomegalovirus, HIV, toxoplasma)

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21
Q

What happens during infectious mononucleosis?

A

Infectious mononucleosis caused by 1° infection with EBV only occurs in minority of patients - infection is subclinical
Lymphocytosis - Clonal expansion of T cells reacting against B cells infected with EBV

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22
Q

What is an overview of EOSINOPHILIC LEUCOCYTOSIS
(eosinophilia)?

A

> 0.4x10^9/L
If > 1.5x10^9/L for over 6 months with tissue damage and no underlying cause = hypereosinophilic syndrome

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23
Q

What are causes of eosinophilia?

A

allergic reactions
parasitic diseases (e.g. amoebiasis, hookwoom, tapeworm infestation)
Metastatic malignancy with tumour necrosis
GM-CSF treatment

24
Q

What are primary B cell immunodeficiencies?

A

X-linked agammaglobulinaemia, acquired common variable hypogammaglobulinaemia, selective IgA or IgG subclass deficiencies

25
Q

What are primary T cell immunodeficiencies?

A

Thymic aplasia (DiGeorge’s syndrome), PNP deficiency

26
Q

What are primary T and B cell immunodeficiencies?

A

SCID (ADA deficiency or other cause), Bloom’s syndrome, ataxia-telangiectasia, Wiskott-Aldrich syndrome

27
Q

What are secondary B cell immunodeficiencies?

A

Myeloma, nephrotic syndrome, protein-losing enteropathy

28
Q

What are secondary T cell immunodeficiencies?

A

AIDS, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, drugs, steroids, ciclosporin, azathioprine, fludarabine

29
Q

What are primary T and B cell immunodeficiencies?

A

Mixed B and T cell Chronic lymphocytic leukaemia, post-bone marrow transplantation and post chemotherapy / radiotherapy

30
Q

What are differences between B and T cells?

A

Origin - T cell (thymus) or B cell (bone marrow)
Tissue - T cell (distribution parafollicular areas of cortex in
nodes, para-arterioloar in spleen) B cell (germinal centres of lymph nodes, spleen, respiratory tract)
Blood - B cell (80% of lymphocytes; CD4>CD8) T cell (20% of lymphocytes)

31
Q

What is the fuction of B and T cells?

A

Function - B cell CD8+ (cell mediated immunity against intracellular organisms) or CD4+ (T cell help for Ab)
B cell humoral immunity via generation of antibodies)

32
Q

What are characteristic surface markers of B and T cells?

A

B cell: CD1, CD2, CD3 and CD4 or 8
T cell: CD19, CD20, CD22, CD9 (pre B cells), CD10 (precursor B cells)
Both MHC class I and II

33
Q

What genes are rearranged for B and T cells?

A

T cell - TCRa, b, g, d
B cell - IgH, Igk, Igl

34
Q

What is lymphocytosis?

A

Normal lymphocyte cell count: 1.5 - 3.5x10^9/L
Absolute lymphocytosis when count > 4.0x10^9/L
Relative lymphocytosis = higher proportion (> 40%) of lymphocytes among the white blood cells, but, absolute lymphocyte count (ALC) is normal
Often occurs in infants and young children in response to
infections that produce neutrophil response in adults

35
Q

What can cause lymphocytosis?

A

Infections:
* acute - infectious mononucleosis, rubella, pertussis, mumps,
HIV, herpes simplex
* chronic - tuberculosis, toxoplasmosis, syphilis

Chronic lymphocytic leukemia (CLL), acute lymphoblastic leukemia (ALL), non-Hodgkin’s lymphoma, thyrotoxicosis

36
Q

What are localised causes of lymphadenopathy (enlarged lymph nodes)?

A

Local infection
Lymphoma
Carcinoma (2°)

37
Q

What are generalised causes of lymphadenopathy (enlarged lymph nodes)?

A

Infection (viral (e.g. measles), bacterial (e.g. syphilis), fungal (e.g. histoplasmosis), protozoal (e.g. toxoplasmosis))
Non-infectious inflammatory disease (e.g. sarcoidosis)
Malignant (e.g. leukaemias)
Miscellaneous (e.g. reaction to drugs, hyperthyroidism)

38
Q

What is an overview of lymphopenia?

A

LYMPHOPENIA or sometimes termed lymphocytopenia
Abnormally low level of lymphocytes
Also a natural consequence of ageing (atrophy of thymus)

39
Q
A
40
Q

What are examples of inherited immunodeficiency diseases?

A

RAG1/2 and Artermis - V(D)J recombination
DiGeorge syndrome - thymus development
AID - Ig class switch and hypermutation
TAP1/TAP2 - cytotoxic T cell antigen recognition
Factor H/I - major functions of the complement

41
Q

What is the normal hypersensite reaction?

A

Immune response mobilizes a number of effector molecules to remove antigen
Localised inflammatory response

42
Q

What can go wrong with the hypersensitivity reactions?

A

Inflammatory response can have deleterious effects -
significant tissue injury, serious disease, death

43
Q

What is an overview of hypersensitive development?

A

Hypersensitivity reactions may develop in the course of either a humoral or cell-mediated immune response

44
Q

What is an overview of anaphylatic reaction?

A

Anaphylactic reactions triggered by antibody or antigenantibody complexes are Immediate Hypersensitivity (minutes/hours)

45
Q

What is an delayed-type hypersensitivity?

A

Delay of symptoms until days after exposure

46
Q

How many types of hypersensitivity are there?

A

4

47
Q

What are organ specific autoimmune diseases?

A

Addison’s disease - adrenal cells - auto-antibodies
Graves’ disease - Thyroid-stimulating hormone receptor - autoantibodies
Mycocardianl infarction - heart - autoantibodies
Hashimoto’s thyroiditis - throid proteins and cells - Th1 cell

48
Q

What are systemic autoimmune diseases?

A

Ankylosing spondylitis - vertebrae - immune complex
MC - brain or white matter - TH1 cells, Tc cells and autoantibodies
Scleroderma - nuclei, heart, lungs and kidney - auto-antibodies

49
Q

What is an overview of Type 1 hypersensitivity?

A

Immune cells recognise non threatening molecules secreting IgE activating mast cells
Mast cells degranulate releasing vascoactive amines which cause problems
Seen with anaphylaxis, asthma, hayfever and eczema

50
Q

What is an overview of Type 2 hypersensitivity?

A

Ab bound to cell surface antigen can activate complement
=> MAC
Cytotoxic cells with Fc receptors bind to Fc region of Ab on target cells and promote the killing of the cells - ADCC
Ab bound to foreign cell can also serve as an opsonin, promoting phagocytosis

51
Q

What is an overview of Hemolytic disease?

A

Maternal IgG antibodies specific for foetal blood-group antigens cross the placenta and destroy foetal red
blood cells
Rh+ fetus and Rh- mother = common

52
Q

What is an overview of type III sensitivity?

A

Reaction of Ab with Ag generates immune complexes usually facilitates clearance by phagocytic cells
Large amounts of immune complexes can lead to tissue damaging type III reactions
Localised or widespread (immune complexes carried by blood)

53
Q

What is an overview of complexes with type III sensitivity?

A

Immune complexes activate the complement system’s array of mediators
C3a and C5a are anaphylatoxins (local mast-cell degranulation and increased vascular permeability)
C3a, C5a and C5b67 - chemotactic factors for neutrophils => degranulate => tissue damage

54
Q

What are examples of type III hypersensitivity?

A

Localised immune complexes mediate an acute Arthus reaction:
‘farmer’s lung’
‘pigeon fancier’s disease’

55
Q

What is an overview of type IV hypersensitivy?

A

Subpopulations of TH cells on encounter with Ag secrete
cytokines that induce localised inflammatory reaction called DTH
Large influxes of non-specific inflammatory cells (macrophages)
Robert Koch - ‘tuberculin reaction’
characteristic skin lesion

56
Q
A

3s2: Infection and Immunity (12 decks)

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