5.7. Immune system Flashcards
What is a pathogen?
a disease-causing agent – can be viruses, bacteria, fungi, protoctists, animals, plants (only to other plants) – no Archeans
What can pathogens be regarding their host “preferences”? give examples. How are those second diseases called in case of animals?
species-specific or can cross species barriers (changing their receptors to fit other cell glycoproteins) like rabies virus, SIV (HIV), tuberculosis, COVID-19…
Zoonosis is a disease that can be transmitted from an infected animal to a non-infected human
Human immune system organs and tissues and their function
Immune cells develop in bone marrow (B-lymphocyte) and thymus (T-ly)
Lymph nodes strategically positioned to prevent the pathogens from entering the trunk where vital organs are situated
Tonsils
Spleen
Appendix (storage of immune cells/tissue at the appendix – impaired flow unlike in the rest of the long intestine, accumulation of pathogens)
Two immune systems:
- Innate/non-specific IS – 1st line of defense skin and mucous, 2nd line macrophages (phagocytes)
- Adaptive/specific IS (not inherited) 3rd line of defense mediated by T-ly and B-lymphocyte cells
How do skin and mucous prevent the entry of microbes
Epidermis (20-30 cells, physical barrier, carotin, dead cells, acidic) and dermis (thicker, tissue-specific STEM cells that renew skin, acidic due to sebum (produced by sebaceous gland, made of lactic and fatty acid)
Mucous membrane protects internal cavities that are exposed to the external environment, contains lysozyme that destroys the bacterial cell wall (peptidoglycan)
White blood cell types:
- majority of leukocytes are outside of blood, in the lymph or interstitial fluid
Neutrophils – phagocytes
Monocytes (macrophages, phagocytes/phagocytic leukocytes) – cells in the interstitial space that recognize pathogens by their AG, perform phagocytosis (lysosome inside) and alarm the 3rd line of defense – move by amoebal movement (arms to swim)
Eosinophil
Basophil
Lymphocytes (B and T cells)
Wound process:
Pathogens enter through skin
Leukocytes in blood recognize chemicals released by pathogens and injured cells
Leukocytes exit through capillary cell wall and follow chemical signals
At the site of damaged tissue, monocytes differentiate into macrophages and start phagocytosis
Eosinophils and neutrophils also release chemicals that digest pathogens (and phagocytosis)
Phagocytosis process
Lysosome, vessel with pathogen, fuse
End products of digestion expelled by exocytosis except AG
AG displayed on the plasma membrane, connected to an MHCH protein (major human histocompatibility complex) – cell is turned into an antigen-presenting cell (APC)
Antigens function
Intramembrane protein
Basis for the distinction between self- and non-self cells is antigens (glycoproteins).
Structure genetically controlled so close relatives have more similar AGs
When a pathogen enters the body, AG is what the immune system reacts against
RBC groups and antigens
Blood transfusion: immune response triggered by recognition of non-self AG on erythrocyte membrane
ABO: 0 (AG H, all RBC possess it), A (AG H + a sugar), B (AG H + an amine), AB (AG H, sugar and amine)
0 has anti-A and anti-B antibody, A only anti-B, B only anti-A, AB none – 0 is universal donor, AB universal acceptor – AB in the plasma
Rh: Rh+ (AG Rh), Rh-(don’t have AG Rh)
Rh+ has no AB, Rh- has anti-Rh AB
Rh AG developed only contact made with Rh+ and genetic potential for Rh-
Antibodies structure and function
Immunoglobulins
Proteins that recognize and bind to specific AG on a pathogen – specific to only one AG (every human has millions of different types of lymphocytes)
Mobile and soluble unlike AG
4 polypeptide chains joined together (cystine by disulfide bridges) to form a Y-shaped structure with a constant and a variable region. The AG binding site is on the tips of variable regions (specific, unique a-a sequence)
AB destroy pathogens by (3 ways):
- Neutralization – blocks viral binding sites and coats bacteria (membrane created)– prevents binding and thus replicating – marks it for phagocytosis
- Creating holes on the pathogen’s membrane
- Agglutination of microbes – marking them for destruction by making them larger and less mobile, easier target for phagocytes – one AB binds to AG of two pathogens
Immune response/AB production
- Phagocytes perform the phagocytosis
- AG presentation – APC created from phagocytic leukocyte
- Activation of helper T-ly – recognize and bind to AG on macrophage which activates it
- Activated T-helper activates B-ly cells to confirm AG’s presence, if the rsceptor on B-ly is complementary to the AG, B-ly is activated by cytokines from helper T-cell
- Activated B-ly creates either plasma cells (enlarged B-cell clones with an extensive rER to produce AB in order to fight the infection) or memory cells (stay the same and wait for another infection when they immediately react and proliferate and produce AB, without T-cells. The stronger the infection, the stronger the developed immunity (more memory cells) and they either last for a few years or forever)
How is the secondary response different from the primary?
much faster and more intense because a large number of memory cells has remained after the 1st infection and they are capable of producing large amounts of AB very quickly when stimulated by an AG
What are and what is the reason for the existence of polyclonal and monoclonal AB? Example of one (pregnancy kit).
Polyclonal – most pathogens have more than one AG, stimulat more than one type of lymphocyte and thus result in production of more than one AB – produced any time the infection is natural
Monoclonal – only possible by vaccination – basis for tests (COVID, pregnancy) and treatments (tetanus, venomous bite)
Test based on detecting the human chorionic gonadotropin (hCG) hormone (early pregnancy) – firstly, hCG joins with artificial monoclonal AB, if the hormone’s present, immobilized monoclonal AB inside the test join with it, the joining causes a change in color – the second window exists to ensure that the test works, third type of monoclonal AB joins with empty AB (after the first window)
