This document summarizes key concepts in immunology as they relate to periodontal disease. It discusses the epithelial barrier and pattern recognition receptors that detect pathogens. Inflammatory mediators recruit immune cells through chemotaxis. T lymphocytes develop and differentiate into subsets like Th1, Th2, Th17 that activate different immune responses. B cells produce antibodies through somatic hypermutation. Regulatory T cells control self-tolerance. The adaptive response becomes antigen-specific and develops memory. Dendritic cells present antigens to activate T cells. An imbalance in T cell subsets can lead to tissue destruction in periodontal disease.
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summary of factors contributing to the pathogeesis of SLE and the events that lead to its associated tissue damage, from genetic and immunologic point of view
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51. TH1/TH2
• Adoptive transfer of specific T helper type 1 or
type 2 cells into nude rats .
• In these experiments, T helper type 2 cells were
found to protect the periodontal tissues from
destruction by bacterial infection while the type 1
cells did not.
• Furthermore, antibodies to P. gingivalis reduced
the virulence of this pathogen in animal models .
52. • Immune modulation can be achieved
either by using
• 1) immunization protocols that would
favor a T helper type 2 response
(primary immune response)
• 2) by introducing T helper type 2
cytokines directly in the local lesion
(secondary immune response).
57. WHY SHIFT IN THE Th PARADIGM
• 1.Many cytokines origin cannot be explained by
Th1&2
• 2.Certain species produce only IL-17
• 3.Resistance to certain diseases inspite of Th1&2
• 4.PGE2 increase IL-23 & inhibit IL-12
• 5.No consensus on Th1&2 and disease
progression
• 6.Associated bone loss
61. 17A ----17 F
• The IL-17 family play a role in a number of
diseases
• Rheumatoid arthritis
• Pulmonary disease
• Lupus
• Multiple sclerosis
• IBD
62. TH17 in periodontitis
• Pro – and anti inflammatory property
• Stimulate epithelial,endothelial
&fibroblast to produce IL-6,IL-8 & PGE2
• Primary source of RANKL
65. CYTOTOXIC (KILLER )
T LYMPHOCYTES
• Tc1 -- IFN ,TNF
• Tc2 -- IL-4 ,IL-5
• SUPRA MOLECULAR ACTIVATION CLUSTER (SMAC )
• Actin reorganisation
• Position lytic granules to the target cell contact site
• Perforin form pores
• Granzyme enter & cleaves
• Involve cell surface receptors ( FAS ligand –FasL )
• FasL – Fas – FADD -- CASPASE
66.
67. B- cells
• B cells divided into B-1a & B-1b
• B-1a express CD5 .Specific sites . Early T –cell independent
• Low affinity
B1a --- from peripheral blood of patients with auto immune
diseases
• Produce IgM autoantibodies
• Marker of susceptibility
• No decrease in level after therapy
68. B2 --- from bone marrow .CONVENTIONAL B
CELLS.
T-dependent
Yield isotype swiched high affinity memory
cells & plasma cells .
Periodontitis have B-1a & B-2 .
Internalization of antigen by Ig receptor
79. STABLE LESION
TH1 PREDOMINANT
• IFN ENHANCE THE
PHAGOCYTIC ACTIVIT
OF PMN & MO
• CONTAINMENT OF
INFECTION
• LESION PERSISTS DUE
TO CONTINUOUS
FORMATION OF PLAQUE
80. PROGRESSIVE LESION
IF THE INNATE IS POOR ,LOW
IL-12 PRODUCED
,SUPPRESSING TH1
RESPONSE
• TH2 LESION
• B CELLS PLASMA CELLS
• POOR TH1 RESPONSE
,MAST CELL STIMULATION
OF IL-4 =WILL ENCOURAGE
TH2 RESPONSE. , B CELL
ACTIVATION AND ANTIBODY
PRODUCTION
82. REGULATORY T -CELLS
• Suppresses the activation of other cells in
contact dependent or independent manner .
• Interact with both Th1 & Th2 effectoer T
cells and suppress both.
• Which can be thru” APC or direct T-T
interactions
83. TWO MECHANISMS FOR SELF TOLERANCE
:
1.RECESSIVE
2.DOMINANT
REGULATORY T CELLS
IMMUNE TOLERANCE
87. TREG IN PERIODONTITIS
• Nakajima et al. discovered that CD4+ CD25+ regulatory T
cells were present in all healthy ⁄ gingivitis lesions,
although at lower levels than in periodontitis lesions. The
authors speculate that in gingivitis lesions, regulatory T
cells control the immune pathology so as to avoid
periodontal tissue destruction, whereas in established
periodontitis lesions, the regulatory T cells may be
recruited into the lesions in an attempt to suppress
tissue destruction through putative autoimmune
mechanisms via a negative feedback system.
93. STEM CELLS & Th subset
• In vitro & in vivo studies have indicated that
GMSC could significantly inhibit Th17 cells and
simutaneously promote xpansion of nTreg.
Pathogen-associated molecular patterns (PAMPs) are small molecular motifs conserved within a class of microbes, but not present in the host. They are recognized by toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals.