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year 4 CDM 2 > Case 14: Innate & Adaptive immunity > Flashcards

Case 14: Innate & Adaptive immunity Flashcards

1
Q

Definition: Immune system and Immunity

A

Immune system: The organs and processes of the body that provide resistance to infection and toxins.

Immunity: protection from infectious disease and defence against infectious microbes. Identifies the difference between self and non-self.

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2
Q

Innate immune system

A
  • Pre-existing defences: little variation between different humans
  • First line of defence: activates quickly but doesn’t last long
  • Responds to broad types of threats, rather than specific pathogens
  • No change in response with repeated exposure
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3
Q

Adaptive immune system

A
  • recognises and responds to specific threats (specificity)
  • mounts a highly tailored response against specific threat
  • takes time to develop
  • stronger/faster response with repeated exposure (immunological memory)
  • Can very between different people based on exposure
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4
Q

Active immunity

A
  • protection that is produced by an individual’s own immune system and is usually long-lasting
  • acquired by natural disease or vaccination
  • involves generation of adaptive immune responses, resulting in immunological memory
  • Involves B and T cells
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5
Q

Passive immunity

A
  • Protection provided by transfer of antibodies from immune individuals
  • Example: Cross placental transfer from mother-child, blood transfusion, immunoglobulins
  • Temporary protection: weeks or months
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6
Q

Where do blood cells originate from (cell progenitor)

A
  • Myeloid: erythrocytes, platelets, Granulocytes (eosinophils, neutrophils, basophils), Monocytes
  • Lymphoid: B and T cells, Natural killer cells
  • Dendritic cells: Myeloid or lymphoid
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7
Q

Innate immune system: initial barriers

A
  • Physical barriers: skin, mucous membranes in respiratory and GI tract
  • Chemical barriers: acidic pH in GI tract and on skin, enzyme (lysozyme) in tears and saliva
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8
Q

Innate immune system: subsequent protection

A
  • phagocytic cells (neutrophils, macrophages)
  • Eosinophil, Basophil
  • dendritic cells: APC
  • natural killer (NK) cells
  • complement
  • cytokines
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9
Q

Innate immune cells- Granulocyte: Neutrophil

A
  • most numerous leucocytes
  • short lived cells
  • recruited to sites of inflammation
  • take up pathogens (phagocytosis) and destroy them
  • contain numerous ‘granules’ rich in degradative enzymes and anti-microbial substances
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10
Q

Innate immune system- Granulocytes: Eosinophils and Basophils

A
  • Eosinophils: defence against parasites, allergic inflammatory reactions
  • Basophils: defence against parasites, allergic inflammatory reactions
  • Granulocytes: cells which contain granules which can destroy organisms
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11
Q

Innate immune cell: Monocyte

A
  • myeloid derived cells, leave bone marrow
  • circulate in blood
  • can ingest and destroy pathogens (phagocytic)
  • Monocytes are in the blood and then different into Macrophages in the tissues
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12
Q

Innate immune cell: Macrophage

A
  • monocyte derived tissue-based cells
  • engulf and kill pathogens (phagocytic)
  • secrete substances that control inflammation and immunity - cytokines
  • link to adaptive immune response: APC
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13
Q

Innate immune cell: Dendritic cell and Natural killer cell

A
  • Dendritic cell: widespread, ingest and degrade pathogens (phagocytic). Also ingests extracellular fluid- self proteins and present them on a MHC molecule to T cells. Link to adaptive immune system. APC. Site between Myeloid and Lymphoid lineage
  • Natural killer cell: type of ‘large granular’ lymphocyte. Kills infected cells and tumour cells (recognise lack of normal ‘self’) through granules which degrade into anti-microbial substances.
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14
Q

Antigen

A
  • a substance that is recognised and induces an immune system response (e.g. antibody generation)
  • can be a part of a pathogen (e.g. glycoprotein, polysaccharide etc.), toxin, or anything else
  • epitope: the particular part of the antigen recognised by the innate or adaptive immune system receptors
  • Can be a protein, polysaccharide, toxin, DNA, RNA.
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15
Q

Antibody (or immunoglobulin)

A

A protein produced and secreted by B cells in response to an antigen, that is able to specifically bind that antigen making it ineffective

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16
Q

Antigen presenting cells (APC’s)

A
  • These are cells that express MHC class II
  • Help link the innate and adaptive immune system
  • Main cells: Dendritic cells and Macrophages. Can also be B cells
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17
Q

Macrophages role as an APC

A
  • Protein binds to surface of Macrophage
  • Protein is engulfed and broken down with a lysosome enzyme
  • Part of the protein binds to MHC class II
  • This complex moves to the surface of the cell where it can present to other cells i.e. CD4+ T cell
  • The T cell then determines if its self or non-self
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18
Q

Adaptive immune system

A
  • Develops as a response to infection and adapts to it
  • Cell mediated: CD4+ and CD8+ T lymphocytes
  • Humoral: B lymphocytes and antibodies
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19
Q

B and T cells

A
  • Principle cells in adaptive immunity
  • Both have specific receptors: TCR and BCR
  • Which recognise a specific antigen i.e. each T cell produces one specific TCR which recognises one specific antigen
  • Diversity is achieved by having a large number of cells of different specificities
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20
Q

Antibodies

A
  • Produced by B cells
  • Made up of 4 polypeptide chains: 2 identical light chains and 2 identical heavy chains
  • There is a variable region (antigen binding site) and a constant region. Both regions are made from light and heavy chains
  • Variable region changes with different antibodies
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21
Q

T lymphocytes (T cells)

A
  • Each express a T cell receptor of a single specificity
  • TCR is made of 2 different polypeptide chains: most commonly alpha chain and beta chain
  • Variable region (antigen-binding site):
  • Constant region:
  • TCR’s recognise antigens bound to MHC molecules
22
Q

Types of T cells

A
  • CD8+ T cells (cytotoxic):
  • CD4+ T cells (helper)
  • CD4 and CD8 are co-receptors on the surface of T cells which determine if TCR binds to MHC class I or II molecules. They help stabilise the reaction between TCR and the antigen allowing it to occur.
  • Lab uses these surface markers to identify the percentage of each type of T cell (CD4/CD8)
23
Q

CD4+ T cells (T helper cell)

A
  • Recognise antigens bound to MHC class II (only on specialised APC’s)
  • Results in T cell activation and division to form ‘effector cells’ which travel to infection site
  • produce cytokines that direct the immune response
  • their role is to “help” other cells carry out their functions: B cells producing antibodies, Macrophages doing phagocytosis
24
Q

CD8+ T cell (killer cell)

A
  • Kills infected cells (“cytotoxic T cells”). Kills infection and host cell
  • Recognise antigen expressed on the cell surface of all cells by binding to MHC class I (expressed by all cells)
25
Q

B cells

A
  • express B cell receptor, which is a membrane-bound antibody
  • after recognition of their specific antigen on T cells, they secrete antibody’s (main role)
  • Antigen is internalised and broken down. Part of the antigen binds to internal MHC-2 which moves to the surface of the cell. MHC-2 binds with CD4 T cell. The T cell will then help and make the B cell divide and produce lots of antibodies
  • Antibodies provide lifelong protection and are produced from bacteria, viruses, fungi etc
26
Q

Tissues of the immune system: primary

A
  • Central (primary) lymphoid tissue: bone marrow and thymus
  • bone marrow: haematopoesis
  • B cells (along with myeloid cells) produced and develop in the bone marrow
  • T cells produced in the bone marrow and travel to the thymus for maturation and deletion of cells which react to self proteins.
27
Q

Tissues of the immune system: secondary

A
  • Peripheral (secondary) lymphoid tissues: where adaptive immune responses are initiated (lymph node, spleen, mucosal associated lymphoid tissue)
  • dendritic cells migrate from infected tissue to secondary lymphoid organs (e.g. lymph nodes) in lymph via lymphatic vessels where they will come into contact with lymphocytes and activate the adaptive immunity
  • naïve lymphocytes circulate through lymph nodes via the bloodstream
  • Majority of lymphocytes in the secondary lymphoid tissue
28
Q

Circulation of Lymph

A
  • Lymph is extracellular fluid which contains APC’s bringing antigens from tissues
  • Drains from afferent lymphatic vessels into secondary lymphoid tissues (e.g. lymph nodes)
  • fluid (lymph) then leaves lymph nodes via efferent lymphatics vessels, which drain into the thoracic duct
  • this then drains into the bloodstream via the heart
29
Q

Circulation of lymphocytes

A
  • Naive lymphocytes enter the lymph nodes from the blood
  • If they encounter an antigen presented by APC’s they divide to form ‘effector cells’
  • Lymphocytes → efferent lymphatics → lymph nodes → thoracic duct → blood stream
  • activated ‘effector’ cells then go to inflamed tissues (e.g. sites of infection)
  • naïve cells home back to lymph nodes again and continue to circulate between lymph nodes and blood until antigen encountered
30
Q

History of previous infections and PMH

A
  • Site and frequency
  • Pathogens
  • Severity
  • Need for antibiotics
  • Hospital admissions: ITU, involvement of infectious disease team

PMH: Autoimmunity, Malignancy, Immunisation History, Operations (grommets, lobectomies)

31
Q

Infection: family history

A
  • Serious infections
  • Immunodeficiencies
  • Autoimmune diseases
  • Unexplained sudden deaths
32
Q

Medication history (secondary immunodeficiency)

A
  • Lamotrigine can cause a combined immunodeficiency, with viral, fungal and bacterial infections
  • Phenytoin can cause hypogammaglobulinaemia (reduced immunoglobulins) and enlarged lymph nodes that can look like lymphoma (pseudolymphoma)
33
Q

Consider primary immunodeficiencies in adults with:

A
  • > 4 infections requiring antibiotics within one year (otitis, bronchitis, sinusitis, pneumonia)- confirm infection with culture
  • Recurring infections or infection requiring prolonged antibiotic therapy
  • > 2 severe bacterial infections (osteomyelitis, meningitis, septicaemia, cellulitis)
  • > 2 radiologically proven pneumonia within 3 years
  • Infection with an unusual location (liver abscess, osteomyelitis) or pathogen (aspergillus, pneumocystis)
  • Structural damage (bronchiectasis)
  • PID in the family- some are tested for SCID at birth
34
Q

Features associated with immunodeficiency

A
  • Atypical eczema
  • Chronic diarrhoea
  • Failure to thrive
  • Telangiectasia
  • Hepatosplenomegaly
  • Endocrinopathy
  • Chronic osteomyelitis/deep-seated abscesses
  • Mouth ulceration
  • Autoimmunity
  • Family history
35
Q

Associated features with secondary antibody deficiency

A
  • Extremes of age
  • Uraemia
  • Toxins
  • Acute & chronic infections
  • Burns
  • Myotonic dystrophy
  • Protein-losing states
  • Lymphangiectasia
  • Often as a result of medication
36
Q

Immunodeficiency examination

A
  • Weight and height (FTT)
  • Structural damage from infections (ears, lungs, sinuses)
  • Autoimmune features (vitiligo, alopecia, goitre)
  • Absent tonsils (XLA)
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Other potential diagnostic features (telangectasia, eczema)
37
Q

Symptoms with different types of immunodeficiency

A
  • Antibody deficiency: recurrent bacterial chest/sinus infection
  • Neutrophil disorder: recurrent abscesses and unusual organisms
  • SCID and CID: Bacterial, viral and fungal infection
  • Complement deficiencies: recurrent neisserial infections, HUS
38
Q

Most common immunodeficiencies in order

A

B cell, T and B cell together, Phagocyte defects, T cell defect, Complement

39
Q

Causes of liver abscess

A

Neutrophil deficiency

40
Q

Common features in Immunodeficiencies

A
  • increased susceptibility to infection: number or severity
  • susceptibility to cancers i.e. lymphoproliferative disorders
  • can be associated with increased autoimmune diseases
41
Q

10 warning signs of primary immunodeficiency

A
  • > 2 new ear infections within 1 year
  • > 2 sinus infections within 1 year, in the absence of allergy
  • 1 pnuemonia per year for >1 year
  • Chronic diarrhoea with weight loss
  • Recurrent viral infections (colds, herpes, warts, condylomata)
  • Recurrent need for IV antibiotics to clear infection
  • Recurrent, deep abscesses of the skin or internal organs
  • Persistent thrush or fungal infection on skin or elsewhere
  • Infection with normally harmless tuberculosis like bacteria
  • Family history of PI
42
Q

1st line investigations for recurrent infections

A
  • FBC
  • Immunoglobulins: IgG, IgA, IgM
  • Serum electrophoresis: to check for paraproteins or anything that will contribute to a secondary immunodeficiency
  • Lymphocyte surface markers: T cells (CD4+/CD8+), B cells, NK cells. B cell subclasses (naïve, memory, class switched- check if B cells are maturing properly)
  • Specific antibody responses to previous infections
  • Response to immunisation: Tetanus and pneumococcal
43
Q

Immunodeficiency: pathway specific Ix

A
  • Complement pathways: AP100/CH100
  • Neutrophil burst assays i.e. do the Neutrophils work: detects HLH- a life threatening immune disorder of severe inflammation
  • Lymphocyte proliferation assays
  • Genetics: new field, comparing to genetics of previous patients
44
Q

Humoral immunodeficiency

A
  • The most common immunodeficiency: antibody deficiency
  • Present with recurrent bacterial infections which can cause end organ damage i.e. bronchiectasis. Viruses can be cleared
  • recurrent sinopulmonary infections (chest infections)
  • chronic gastrointestinal infections
  • bacteraemia or septicaemia
  • meningitis
  • common pathogens: include the encapsulated bacteria: S. pneumoniae, H. influenzae type b, N. meningitidis. Giardia, cryptosporidium, campylobacter
45
Q

Causes of Humoral immunodeficiency

A
  • All cause antibody reduction
  • selective IgA deficiency (most common)
  • common variable immunodeficiency (CVID)
  • specific antibody deficiency
  • X-linked agammaglobulinaemia (XLA)
  • X-linked lymphoproliferative disease (XLP)
  • hyper IgM syndrome
  • hyper IgE syndrome
46
Q

Medications and Malignancies which reduce antibodies

A

Medications which cause reduced production of antibodies: Prednisolone, Azathioprine, Methotrexate, Rituximab, antiepileptics, antipsychotics

Malignancies which cause reduced production of antibodies: Myeloma, Lymphoma, Leukaemia

47
Q

Hypogammaglobulinaemia

A
  • Antibody deficiency
  • Selective IgA deficiency: relatively common, only needs further investigations if recurrent infections
  • If its due to increased losses i.e. through the gut more likely to have deficiency in IgG
  • Low IgM in old age is common/normal
48
Q

Reasons for low Ig (antibody levels) general

A
  • Reduced production: primary or secondary (medication)
  • Increased losses: Kidneys (nephrotic syndrome), GI (coeliac disease, IBD), peritoneal dialysis
49
Q

Investigations for Humoral deficiency

A
  • response to vaccines
  • lymphocyte surface markers
  • immunoglobulins
50
Q

Assessing response to immunisation

A
  • Done when you suspect an Humoral deficiency but there Immunoglobulin levels are normal so need to check function
  • Polysaccharide vaccine: more difficult to make an immune response to. If the patient has no Pneumococcal IgG antibodies we can give Pneumovax (vaccine) and check Pneumococcal IgG 4-6 weeks later. Serotypes or total. If good response then its re-assuring
  • Protein vaccine: easier to generate an immune response so less useful. Tetanus and diptheria IgG, pneumococcal IgG antibodies (Prevener- conjugated vaccine)
  • Check baseline serology, give vaccine, assess antibody levels 4-6 weeks later
51
Q

Assessing vaccine response

A
  • Specific antibody deficiency= Diagnosis is made on the failure to respond to pneumococcal vaccination (Pneumovax)
  • Normally: would have >4 fold increase after 4-6 weeks
  • Beware failure to maintain protective specific antibodies beyond 6 months
  • If Conjugated Pneumococcal vaccine expect to respond to >7 serotypes (more complicated)

year 4 CDM 2 (39 decks)

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