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.
