CURRICULUM VITAE

Nama : dr. AGUS JOKO SUSANTO, SpPD, K-AI, FINASIM

Tempat/tanggal lahir : Wonogiri, 6 Desember 1973
Agama : Islam
Istri : dr. Dyah Rohmania Agustiana
Alamat kantor : Divisi Alergi Imunologi Klinik-KSM Ilmu Penyakit Dalam
RSUD dr. Moewardi/FK UNS Surakarta
Alamat rumah : Jl. Garuda 43 RT 1/RW 2 Triyagan, Mojolaban, Sukoharjo
Email : agusjoko.susanto4@gmail.com

RIWAYAT PENDIDIKAN

1. Dokter umum Tahun 1999 FK UNS Surakarta

2. Dokter Spesialis Penyakit Dalam Tahun 2010 FK UNS Surakarta
3. Dokter Spesialis Konsultan Tahun 2017 FK UI Jakarta
Alergi Imunologi Klinik

RIWAYAT PEKERJAAN

Tahun Nama Instansi Jabatan

Tahun 1999-2000 RS Keluarga Ibu, Tangerang Dokter Umum

Tahun 2000-2003 Puskesmas Pagerbarang, Tegal Kepala Puskesmas
Tahun 2003-2005 RSI Muhammadiyah Dokter Umum
Jatibarang, Brebes
Tahun 2003-2005 Bapel JPKM Kabupaten Tegal Kepala Bapel JPKM
Tahun 2010-2012 Bagian IPD RSUP dr. Sardjito/ Staf Bagian
FK UGM Yogyakarta
Tahun 2013-Sekarang Bagian IPD RSUD dr. Moewardi/ Ketua Divisi Alergi
FK UNS Surakarta Imunologi Klinik
Tahun 2013-Sekarang Tim Pelaksana Uji Coba Kurikulum Anggota
Pendidikan Klinis FK UNS
Tahun 2014-2015 Program Studi Profesi Dokter FK Sekretaris
UNS
Tahun 2014-Sekarang Tim Perawatan Paliatif RS Moewardi Anggota
Tahun 2017-Sekarang Tim Verifikator Internal RSDM Anggota

KEANGGOTAAN

Keanggotaan Tahun
PAPDI Cabang Surakarta 2010
PERALMUNI Cabang Surakarta 2015
IDI Cabang Sukoharjo 2008
FINASIM 2014
PERALMUNI Indonesia 2015

4. Program Pasca Sarjana S3 Mulai Tahun 2018 FK UNS Surakarta

Riwayat Pekerjaan
Tahun Nama Instansi Jabatan
 
Tahun 2018-sekarang RS Dr Moewardi Gedung Flamboyan Kepala Instalasi
Flamboyan
Tahun 2018-sekarang Tim Akreditasi RS Moewardi Ketua Pokja ARK
Tahun 2017-2018 Tim Verifikator Internal RS Moewardi Anggota
Tahun 2014-2017 Tim Perawatan Paliatif RS Moewardi Anggota
Tahun 2014-2015 Program Studi Profesi Dokter FK UNS Sekretaris Prodi
Tahun 2013-Sekarang Tim Pelaksana Uji Coba Kurikulum Anggota
Pendidikan Klinis FK UNS  
Tahun 2013-Sekarang SMF IPD RSUD dr. Moewardi/ Ketua Divisi Alergi
FK UNS Surakarta Imunologi Klinik
Tahun 2010-2012 Bagian IPD RSUP dr. Sardjito/ Staf Bagian IPD
FK UGM Yogyakarta
Tahun 2003-2005 Bapel JPKM Kabupaten Tegal Kepala Bapel JPKM
Tahun 2003-2005 RSI Muhammadiyah Dokter Umum
Jatibarang, Brebes
Tahun 2000-2003 Puskesmas Pagerbarang, Tegal Kepala Puskesmas
Tahun 1999-2000 RS Keluarga Ibu, Tangerang Dokter Umum

Keanggotaan Mulai Tahun

Ketua Dewan Pembina Yayasan Autoimun BARLINGMASCAKEBES   2018-sekarang

Dewan Pembina Yayasan Sjogren’s Sindrom Indonesia 2018-sekarang
EAACI Alergi Imunologi Eropa 2017-sekarang 
PERALMUNI Indonesia 2015-sekarang
PERALMUNI Cabang Surakarta 2015-sekarang
FINASIM 2014-sekarang
PAPDI Cabang Surakarta 2010-sekarang
IDI Cabang Sukoharjo 2008-sekarang
IMMUNODEFICIENCY IN SEPSIS

  

  
AGUS JOKO SUSANTO

Allergy and Clinical Immunology Division

Internal Department-Moewardi Hospital/Sebelas Maret University, Surakarta
 IMMUNE SYSTEM

AGUS JOKO S, 2019

AGUS JOKO S, 2019
 IMMUNODEFICIENCY

AGUS JOKO S, 2019

 Classification

The International Union of

Immunological Societies
(IUIS)

AGUS JOKO S, 2019

 Immunodeficiency

- Primary

- Secondary

  
AGUS JOKO S, 2019
 Primary Immunodeficiency

 Primary immunodeficiency diseases (PIDs) are a group of

disorders caused by basic defects in immune function of the cells
and proteins of the immune system.

 There are more than 350 types of PIDs. Some are relatively
common, while others are quite rare. Some affect a single cell or
protein of the immune system and others may affect two or more
components of the immune system.

AGUS JOKO S, 2019

 Secondary Immunodeficiency

1. Surgical manipulation (Lymphoid organs,

Bursa Fabricius / Thymus)
2. Ionizing Radiation
Radiation damages DNA
3. Chemical & biologic Immunosuppressive agents
AGUS JOKO S, 2019
 4. Corticosteroids ( Immuno Suppressive )

a. Decreasing the binding of immune

complexes to Fc and C3b receptors of phagocytic cells.
b. Depressing bacterial activity, antigen –
processing activity and IL1 production by macrophage
c. Depressing the release various lymphokines
5. Malignancies
6. Infections
a. Measles and other certain other viral diseases
b. HIV
c. TBC
AGUS JOKO S, 2019
 IMMUNODEFICIENCY IN SEPSIS

AGUS JOKO S, 2019

 SEPSIS

Defined as ‘life-threatening organ dysfunction caused

by a dysregulated host response to infection’.

Sepsis is associated with a strong activation of the

immune system, by stimulation of PRRs by PAMPs
and DAMPs, leading to the activation of target genes
coding for proinflammatory cytokines such as tumor
necrosis factor (TNF), IL-1β, IL-12, and IL-18.
(Luuk Giesen and Mervyn Singer, Handbook of Sepsis; 2018,p:3-14)
 Sepsis Severe or Septic Shock

 Immunodeficiency is common in patients with severe sepsis or septic

shock.

 Despite a similar crude mortality, immunodeficiency was associated

with an increased risk of short-term mortality after multivariate
analysis. Neutropenia and specific, but not all, profiles of
immunodeficiency were independently associated with an increased
risk of death.

CHEST 2014; 146( 5 ): 1205 - 1213

 Sepsis-associated immune suppression involves
several cell types

 Massive apoptosis leads to depletion  This depletion is seen in lymphoid

of immune cells, especially CD4+ organs and body sites, such as the
and CD8+ T cells and B cells spleen, thymus, lymph nodes, and
gut-associated lymphoid tissue

(T. S. R. van Engelen et al., Handbook of Sepsis; 2018,p:33-40)

 Accelerated Apoptosis of
Memory B Cells

AGUS JOKO S, 2019

 (Crit Care Med 2017; 45:875–882)
AGUS JOKO S, 2019
Sepsis-associated B-cell depletion occurs with normal
survival factor concentrations
Admission (D1) and final day (DF) absolute B-cell count
shows significantly lower counts in sepsis patients
(Crit Care Med 2017; 45:875–882)
B-cell apoptosis in sepsis was proportionally higher in memory B-lymphocyte
subsets and associated with higher mean fluorescent intensity.

(Crit Care Med 2017; 45:875–882)

 Long-lasting impairments in
CD4+ T-cell responses

AGUS JOKO S, 2019

The reactivity of immune cells to different activators appears to be comprehensively impaired
in survivors of sepsis. Among other reasons, this could be based on the downregulation of
distinct cell surface receptors.

(Arens et al, Critical Care 2016; 20: 93)

(Christoph Ammer-Herrmenau et al, Plos One 2019; 1-16)
The loss of T lymphocytes in acute sepsis is followed
by a rapid and sustained increase in T-lymphocyte
numbers Recovery of naive and effector/memory
T lymphocytes after sepsis
(Christoph Ammer-Herrmenau et al, Plos One 2019; 1-16)
 Data thus far have shown that the overall number
of T lymphocytes as well as the CD4+ and CD8+
subpopulations including the naive T cells have
largely returned to normal values 3.5 months after
sepsis.

The recovery of T cell populations could be due to

increased thymic output after sepsis or to
homeostatic proliferation of those T cell clones
which survived during sepsis.

Repopulation of the peripheral T cell pool by

recent thymic emigrants (RTEs) after sepsis

(Christoph Ammer-Herrmenau et al, Plos One 2019; 1-16)

 Secondary infections, including fungal
infections, contribute significantly to
sepsis mortality.

Efficient T-cell responses against

pathogens do not only rely on a broad
TCR repertoire but also on the swift
induction of the appropriate effector
functions.

Impaired Th-cell response to fungal antigen after sepsis

(Christoph Ammer-Herrmenau et al, Plos One 2019; 1-16)

 Sepsis-Induced Osteoblast
Ablation

AGUS JOKO S, 2019

Reduction of the CLP Number in the Osteoblast-Ablated Mice
Sepsis-Induced Bone
Loss Is Independent of
the MyD88 and TRIF
Pathway
IL-7 Derived from Osteoblasts
Accounts for Lymphopoiesis
MATUR NUWUN