Immune Cells Flashcards
Where do all immune cells originate
Bone marrow (including B and T cells)
Where do T cells mature
The thymus + thymus tolerance
Lymph nodes are where…
APC + T/B cell interactions
B and T cells can accumulate - lymphomas can cause enlarged, rubbery lymph nodes
The spleen is where…
RBCs are removed - leukaemia’s can cause splenomegaly
Innate immune response
NON-SPECIFIC, RAPID, ALREADY ACTIVE defence system you were born with e.g. mucus or inflammation
NO MEMORY
Killing usually: COMPLEMENT ACTIVATION
Neutrophil + macrophage mostly
* physical barriers - skin, mucus, cilia
* chemical barriers - lysosome in tears, stomach acid
Adaptive immunity response
SPECIFIC, SLOW, NEED ACTIVATION, HAVE MEMORY Acquired defence system to destroy/ prevent growth of pathogens e.g. antibiotics
Killing usually ANTIBODY MEDIATED
B (and plasma cells and antibodies) and T cells are part of the adaptive immune response. The rest is part of the innate immune system
Complement system
Destroy foreign antigens by:
- DIRECT LYSIS: membrane attack complex for station (MAC)
- OPSONISATION: increases phagocytosis (c36)
- INFLAMMATION: macrophage chemotaxis (c3a + c5a)
Neutrophils role (Innate cells)
Most abundant WBC (70%)
Hours to days
Express CD66 receptors (common for all granulocytes)
Phagocytic
Mainly involved in acute inflammation
Macrophages roles (Innate cells)
Months - Years
When monocytes migrate from blood to tissue they become macrophages
Phagocytosis, antigen presenting, cytokine secretion
Clear apoptotic debris
Have TLRs, complement receptors, and Abs bound by Fc portion of receptor
Basophils + mast cell role (innate cells)
IgE binding = degranulation = HISTAMINE release
T1 HYPERSENSITIVITY
Involved in allergic reactions, eczema, hay fever
Basophils = Circulating in body
Mast Cells = Fixed at tissue
Eosinophil’s role (innate cells)
Contain major basic protein
Involved in parasitic infections
NK cell (innate cells)
Release lytic granules that kill virus infected cells
Activation = degranulation = PERFORIN (perforates viral infected cells)
Also involved in malignant cell killing
PAMPs
Pathogen associated molecular patterns - they are recognized by pattern recognition receptors (PRRs) on the phagocytes during phagocytes e.g. toll like receptors
PRRs
Antimicrobial peptides secreted in lining fluids, from epithelia and phagocytes. Examples being:
(TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs), AIM2-like receptors (ALRs), C-type lectin receptors (CLRs), and intracellular DNA sensors such as cGAS
APCs
Interfere between innate and adaptive immunity
These cells process and present antigens from pathogens from recognition to Th cells, to stimulate further Th proliferation, and stimulate B cell production -> ANTIBODIES. When dendritic cell + Th cells communicate = IMMUNE SYNAPSE
3 conditions must be met here to function
1. RECEPTOR BINDING
2. CO-STIMULATION (other molecules bind after 1’ receptor binding)
3. CYTOKINE RELEASE
e.g T cells
Dendritic cells, however macrophages and B cells are also APCs
T helper cells (adaptive cells)
Maturation in thymus (after BM production)
T helper cells
Help activate B cells and cytotoxic T cells
Cytotoxic T cells (adaptive cells)
Can express CD8
Release perforin that causes cells to lyse
B cells (adaptive cells)
Maturation and production in BM
CD20 is the mature cell marker. Monoclonal antibodies (e.g Rituximab) target CD20
Activation:
1. Th2 activated by APC binding + MHC II interaction
2. Th2 releases:
- IL4 which induces B cell proliferation (clonal expansion)
- IL5 which induces B cell differentiation into plasma cell = produce gamed Ig’s
Activated B cells become plasma cells that then produce antibodies
Role of antibodies
Neutralise toxins
Opsonisation of pathogens
Destroy pathogens
IgA function and features
Most Abundant Ig in total body
The mucosal Ab as a dimer. Present in colostrum/ breast milk and coats neonate gut
IgM function and features
First Ig released in ADAPTIVE IMMUNITY
Less response specific
Pentameric and not entirely specific to antigen. Highest capability to activate complement
IgG function and features
Most abundant in the blood. Highly specific. Important during secondary responses, marker of immunological memory. 4 subclasses. Can cross the placenta
IgE
Bound to Mast cells and basophils by FcεR. Important in allergy and helminth infection. Least abundant in the blood
T1 HYPERSENSITIVITY REACTION (ANAPHYLAXIS)
IgD
Not that important. Function is debated in the literature.
Type 1 hypersensitivity reaction mechanism- ANAPHYLAXIS
Antigen reacts with IgE bound to mast/basophil cells = degranulation = histamine release
- Effects: vaso dilation, increased permeability (H1 receptor), broncho-constriction, facial flush, pruritis, swollen tongue and face
E.g. Anaphylaxis, Atopy (asthma, eczema, and hayfever)
Type 2 hypersensitivity reaction - ANTIGEN-ANTIBODY COMPLEX
IgG or IgM binds to antigen on cell surface and activates MAC (complement) AT SITE of A-A binding
E.g. Autoimmune haemolytic anaemia, Goodpasture’s syndrome, pernicious anaemia, rheumatic fever
Type 3 hypersensitivity reaction - IMMUNE COMPLEX DEPOSITION
Free antigen and antibody (IgG, IgA) combine and activates complement at site of A-A deposition
E.g. Systemic lupus erythematous, post-streptococcal glomerulonephritis
Type 4 hypersensitivity reaction - CELL MEDIATED
T cell mediated
TH1 activated by APCs = response
E.g Tuberculosis, graft versus host defence, multiple sclerosis, guillian-barre syndrome
Treatment of anaphylaxis
ABCDE - IM adrenaline - IV fluids, resus
Chlorophenamine (anti-histamine) and hydrocortisone (cortisol) can be used too
Active immunity
Produced by the host immune system
Induced by infection or vaccines
Durable effective protection
Effective after initial lag period
Immunological memory is present
Boosted effect on subsequent dose
Negative phase
