Lectue #8 Flashcards
Extra cellular bacteria
-Innate immunity
Complement (MAC and opsonization)
Phagocytosis
NETosis
Extra cellular bacteria
-Adaptive immunity
B cell activation IgM at the beginning,
then isotype switching by Th2 to IgG or IgA
-Mucosal immunity IgA provide neutralization
-Interstitial immunity IgM and IgG provide neutrilization, opsonization and complement activation
Extra cellular bacteria
-Tissue injury
Directly by endo and exotoxins
Indirectly by complement activation
Extra cellular bacteria
-Evading the immune system
Antigentic variations
Sialic acid capsule
Extra cellular vesicles
IgA protease
Extra cellular bacteria
-Peripheral blood shows
-Neutrophilia
In severe infections even “left shift” when premature neutrophils are secreted
-Procalcitonin
Intacellular bacteria
-Innate immunity
NKC can be activated directly or by IL12 from macrophages and neutrophils
Intacellular bacteria
-Adaptive immunity
Th1 activating macrophages and Tc mediated immunity
Intacellular bacteria
-Tissue injury
Due to macrophage activation and granuloma formation
Intacellular bacteria
-Evading the immune system
Unaccessible to complement and antibodies since they are intracellular
Inhibition of phagolysosome formation
Hemolysin secretion
Intacellular bacteria
-Peripheral blood shows
Lymphocytosis and monocytosis
Parasites
-Innate immunity
Resistant to complement system
Macrophages can phagocytose protozoa but not helminths
Eosinophils are the main source of immunity
- Cytotoxic cation proteins: EPO peroxidase, ECP cationic pr, EDN derived neurotoxin, MBP major basic pr
- Cytokines and chemokines:
IL3, 4, 5, 6, 8, 12, 18 IFN gamma, GM-CSF, TGFalpha/beta, VEGF, TNF alpha, eotaxin
- Leukotrienes: LTC4, D4, E4, PAF
- Neuromediators: SP, VIP
Parasites
-Adaptive immunity
IgE Ab
Activation of Th1 and macrophages
Tc for protozoa that survive inside macrophages
Parasites
-Tissue injury
Due to the stimulation of Th1 cells by parasites in the liver - macrophages - granuloma formation
Parasites
-Evading the immune system
Can survive and replicate within the cells
Cyst formation
Tegmentum (capsule like structure)
Certain helminths can activate M2 by cytokine mimicing
or induce DC to activate Treg by polysaccharide secretion
Parasites
-Peripheral blood shows
Eosinophilia with high IgE
Fungi
-Innate immunity
Mainly neutrophils, DC and macrophages
DC will secrete IL23 inducing Th17 and ILC
Fungi
-Adaptive immunity
Th17 Th1
Fungi
-Tissue injury
Macrophage activation, neutrophil degranulation
Fungi
-Evading the immune system
None
Fungi
-Peripheral blood shows
Neutrophilia and in chronic cases monocytosis
Viruses
-Innate immunity
IFN production
1. IFN alpha: by leukocytes as well as by infected cells
2. IFN beta: by fibroblasts as well as by infected cells
IFN alpha and beta signals for the neighboring cells to become virus resistant
3. INF gamma: by NKC (ILC1)
Viruses
-Adaptive immunity
Th2 induce isotype switching of B cells to IgG and neutralization
Th1
Tc
Viruses
-Tissue injury
By the virus and by cytotoxic T cells
Viruses
-Evading the immune system
Antigenic variations (structural plasticity)
-Antigen drift: slight antigen change (few AA substitution)
-Antigen shift: major antigen change (new gene)
Immunosuppression
-MHC modulation: HIV by Nef protein EBV by B2LF2
- Elimination of CTL: by inverting Fas-FasL
Viruses
-Peripheral blood shows
Lymphocytosis (in hepatitis also mononucleosis)
Hyper IgM syndrome
Inability to switch IgM to other classesdue to lack of CD40L on the T cells
Recurrent pyogenic infections will occur
Selective IgA deficiency
Deficiency in serum IgA
Chronig granulomatous disease
Deficiency in NADPH oxidase in neutrophils
AIDS
Acquired immune deficiency syndrome caused by HIV infection
The virus targets CD4+ cells
Its membrane id derived from the host consists of GP160 GP120 GP41
