Respons imun pada bayi dan anak terhadap bakteri.

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The document discusses the immune response in babies and children to bacterial infections. It presents diagrams of the immune system pathways involved in both innate and adaptive immunity. The innate immune response involves cytokines that activate natural killer cells, neutrophils, and macrophages to attack pathogens. The adaptive response involves T helper cells that activate B cells and cytotoxic T cells. Memory cells are also generated to mount a faster response upon future exposures. The mechanisms discussed aid in phagocytosis and lysis of extracellular bacteria through opsonization, complement activation, and Fc receptor binding.

Respons imun pada Bayi dan
Anak terhadap Bakteri.
Prof DR Dr Ariyanto Harsono
SpA(K)

IL-12/ IL-1

Ag

IL-6
TCR

CTL

IL-4

MHC-II

Th0

MHC-I

IL-1

Th-2

B-Cell

IL-2, IFN-γ

TNF-β, IFN-γ

IL-10

Sel Abnormal
FASL

IL-5

I L-2
IFN-γ

Th.1

SEL MEMORI

SEL PLASMA

L

SEL-NK
SEL-NK AKTIF

Memory Cells

FC-R

SITOTOKSIN

ADCC

SEL-LISIS

SEL ABNORMAL

Prof DR Dr Ariyanto Harsono
SpA(K)

2

Th
1
Prof DR Dr Ariyanto Harsono
SpA(K)

(J Allergy Clin Immunol 1999;118:124-6)
4

Prof DR Dr Ariyanto Harsono
SpA(K)

21
Prof DR.dr. Ariyanto Harsono SpAK

Prof DR Dr Ariyanto Harsono
SpA(K)

22
Prof DR.dr. Ariyanto Harsono SpAK

Effectors mechanisms against extracellular
pathogens
OPSONISATION
Bacteria in extracellular space

+
Ab

OPSONISATION

Fc
receptor
binding
Prof DR Dr Ariyanto Harsono SpA(K)

Phagocytosis
27

Effectors mechanisms against extracellular
pathogens
COMPLEMENT Activation
Bacteria in extracellular space

Lysis

+
Ab &
COMPLEMENT

Opsonisation

Complement &
Fc receptor binding
Prof DR Dr Ariyanto Harsono SpA(K)

Phagocytosis
28

INNATE iMMUNITY

Prof DR Dr Ariyanto Harsono SpA(K)

32

Salicylic acid (SA) is the phytohormone required for plant defense against pathogens. Pathogen infection induces SA accumulation in both infested and systemic tissue. Blocking SA accumulation results in the compromised plant immunity, whereas the exogenous application of SA or the SA analogs induces immunity to pathogens. In Arabidopsis, pathogen-induced SA is majorly synthesized through Isochorismate Synthase 1(ICS1/SID2). SARD1 and CBP60g promote pathogen-induced SA synthesis by controlling the expression of ICS1. In addition to ICS1, SARD1 and CBP60g also maintain the expression of a large number of the other immune regulators, suggesting that these two transcription factors play broad roles in the plant immunity. Arabidopsis NPR1 is required for the SA-induced PR gene expression and resistance against pathogens. NPR1 comprises an N-terminal BTB/POZ domain, a central ankyrin-repeat domain and the C-terminal transactivation domain. NPR3 andNPR4 are two paralogs of NPR1 with the very similar domain structures as NPR1

06 isafg p77 genome wide expression consequences of a disease resistance qtl ...

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#67 Análisis genómico comparativo de Clostridium solventogenicos: Una mirada ...

Juan Rosas Morales

Background: Diarrhoeal disease remains a major cause of child morbidity, growth faltering and mortality in low and middle income countries (LMICs), with Campylobacter among the most common causes. Previous work has identified source reservoirs in developed countries (e.g. contaminated poultry or unpasteurised milk), however little is known about the risk factors and transmission routes in LMICs, where incidence is extremely high (up to 85% of children infected before 1yr). Risk factors such as household crowding, poor sanitation, consumption of contaminated water and cohabitation with animals, all constitute potential transmission risks but their relative importance is unknown. Methods: We compare core and accessory genome content within and between infection and source populations by host and region. Signatures of adaptation can be detected in Campylobacter jejuni and C. coli genomes as they recombine and adapt quickly to new hosts. Using sequence data from human clinical isolates and potential source reservoirs we are able to probabilistically attribute sources of infection and model complex transmission networks. Comparative genomics techniques are used to characterise core and accessory genome content within populations and bacterial genome-wide association studies (GWAS) are used to identify disease-severity associated genes and genetic elements. Results: Pilot genomics studies of isolates from humans, animals and food in LMICs have identified genomic variation in strains that may indicate differences in source, survival, transmission or virulence (compared to the UK). Dissemination of homologous accessory genes across Campylobacter lineages in Egypt suggest recent acquisition and spread between hosts. Disease-severity associated genetic elements are identified through a GWAS of isolates from symptomatic and asymptomatic children in the Peruvian Amazon. We also identify novel lineages in isolates from Burkina Faso and high levels of antimicrobial resistance in isolates from Vietnam. Conclusions: Using a global outlook, we have identified differences in the core and accessory genomes of Campylobacter populations that may explain some of the differences we observe in the global epidemiology of campylobacteriosis. As we begin to understand the relationship between the infecting isolate and disease severity, we are able to model transmission networks for appropriate intervention strategies.

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It is commonly assumed high cholesterol contributes to atherosclerosis which initiates with foamy macrophages. Here it is suggested the induction of foam in human macrophages relates instead to the induction of a newly described foamy virus, human endogenous retrovirus K102 (HERV-K102) in response to high cortisol and/or viruses, other intracellular pathogens, or tumors. HERV-K102 is a newly described human host protection mechanism and the particles are replication competent in vitro and in vivo. In healthy or younger adults, the foamy macrophages lyse on day 7 and release the protective HERV-K102 particles. When immunosenescence is evident (associated with low DHEA and high cortisol) the lysis and release of the HERV-K102 particles is blocked by alpha-fetoprotein (AFP). The dysfunctional and partly activated macrophages promote immunosenescence including atherosclerosis. See Laderoute MP, Discovery Medicine article published December 2015 for more details.

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Respons imun pada bayi dan anak terhadap bakteri.

1. Respons imun pada Bayi dan Anak terhadap Bakteri. Prof DR Dr Ariyanto Harsono SpA(K)

2. IL-12/ IL-1 Ag IL-6 TCR CTL IL-4 MHC-II Th0 MHC-I IL-1 Th-2 B-Cell IL-2, IFN-γ TNF-β, IFN-γ IL-10 Sel Abnormal FASL IL-5 I L-2 IFN-γ Th.1 SEL MEMORI SEL PLASMA L SEL-NK SEL-NK AKTIF Memory Cells FC-R SITOTOKSIN ADCC SEL-LISIS SEL ABNORMAL Prof DR Dr Ariyanto Harsono SpA(K) 2

3. Prof DR Dr Ariyanto Harsono SpA(K) 3

4. Th 1 Prof DR Dr Ariyanto Harsono SpA(K) (J Allergy Clin Immunol 1999;118:124-6) 4

5. Prof DR Dr Ariyanto Harsono SpA(K) 5

6. Prof DR Dr Ariyanto Harsono SpA(K) 6

7. Prof DR Dr Ariyanto Harsono SpA(K) 7

8. Prof DR Dr Ariyanto Harsono SpA(K) 8

9. Prof DR Dr Ariyanto Harsono SpA(K) 9

10. Prof DR Dr Ariyanto Harsono SpA(K) 10

11. Prof DR Dr Ariyanto Harsono SpA(K) 11

12. 12 Prof DR Dr Ariyanto Harsono SpA(K)

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18. Prof DR Dr Ariyanto Harsono SpA(K) 18

19. Prof DR Dr Ariyanto Harsono SpA(K) 19

20. Prof DR Dr Ariyanto Harsono SpA(K) 20

21. Prof DR Dr Ariyanto Harsono SpA(K) 21 Prof DR.dr. Ariyanto Harsono SpAK

22. Prof DR Dr Ariyanto Harsono SpA(K) 22 Prof DR.dr. Ariyanto Harsono SpAK

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24. Prof DR Dr Ariyanto Harsono SpA(K) 24

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26. 26 Prof DR Dr Ariyanto Harsono SpA(K)

27. Effectors mechanisms against extracellular pathogens OPSONISATION Bacteria in extracellular space + Ab OPSONISATION Fc receptor binding Prof DR Dr Ariyanto Harsono SpA(K) Phagocytosis 27

28. Effectors mechanisms against extracellular pathogens COMPLEMENT Activation Bacteria in extracellular space Lysis + Ab & COMPLEMENT Opsonisation Complement & Fc receptor binding Prof DR Dr Ariyanto Harsono SpA(K) Phagocytosis 28

29. Prof DR Dr Ariyanto Harsono SpA(K) 29

30. Prof DR Dr Ariyanto Harsono SpA(K) 30

31. Prof DR Dr Ariyanto Harsono SpA(K) 31

32. INNATE iMMUNITY Prof DR Dr Ariyanto Harsono SpA(K) 32

33. Prof DR Dr Ariyanto Harsono SpA(K) 33

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35. Prof DR Dr Ariyanto Harsono SpA(K) 35

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37. Prof DR Dr Ariyanto Harsono SpA(K) 37

38. Terimakasih 38

Respons imun pada bayi dan anak terhadap bakteri.

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