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Table of contents
Avant-propos
Allogeneic hematopoietic stem-cells transplantation
A. Discovery and principle
B. Clinical settings
1. Overview
2. Patient eligibility for alloHSCT
a) Underlying disease impact
b) Individual factors impact
3. Sources of hematopoietic stem cells
4. Donor selection
5. Preparative regimens
6. Post-alloHSCT monitoring
a) Engraftment and chimerism
b) Short- and long-term care
7. Complications and management
a) Relapses and post-alloHSCT secondary malignancies
b) Infectious risk
c) Graft-versus-host disease
(1) Acute
(2) Chronic
(3) Preventive action against GvHD
(a) aGvHD risk factors
(b) Current immunosuppressive prophylaxis
(c) Partial T cell depletion strategies
Immunotherapeutic effect of alloHSCT
A. GvT effect: Definition and clinical evidences
B. Establishment of the alloreactive response
C. Allogeneic effector phase
1. T cells trafficking
2. Effector/memory profile
3. T helper subsets
4. Antigen specificity
5. Cytotoxic mechanisms of tumour cell elimination
D. Causes of relapse
a) Tumour cells intrinsic mechanisms of evasion
b) Microenvironment-induced evasion
E. Clinical strategies for a better GvT effect
1. Toward a relapse prediction
2. Adoptive cell therapies
a) DLI
b) Chimeric antigen receptor T cells
3. Anti-immune checkpoints
The role of regulatory T cells in cancer
A. Fresh perspectives in oncology
B. Treg biology
1. Discovery and key features
2. Treg ontogeny and lineage plasticity
3. Phenotypic characterization
4. Mechanisms of suppression
a) Described suppressing mechanisms
b) Dynamic aspects of Treg suppressive function
5. CD8+ Treg resurgence
C. Treg dysregulation in cancer
1. Treg association with cancer progression
a) State of the art in solid and blood cancers
b) Unravelling the literature divergences
2. Treg interactions with the TME
a) Tumour infiltration and activation
b) Suppression of the anti-tumoral effector response
3. Effect of the current immunotherapies on Treg
D. Interfering with Treg immune suppression
1. Rational behind Treg blockade
2. Indirect anti-Treg strategies
a) Chemotherapeutic agents
b) Induction of “suppression-proof” Teff
3. Treg-specific blockade
a) Freezing Treg migration
b) Bypassing Treg differentiation
c) IL-2/CD25-focused strategies
d) Turning off Treg activation signals
e) Converting Treg into pro-inflammatory cells
The TNF-α/TNFR2 pathway: a new ICP to target
A. Historical point of view
B. Comprehensive overview of TNF- signalling
1. Actors involved and their expression pattern
2. Signalling pathways
C. TNFR2 critical function in tolerance
1. For immune homeostasis maintenance
2. Under inflammatory conditions
D. TNF- implication in alloHSCT
E. TNF-α/TNFR2 role in malignancies
1. In the TME
2. For cancer cells
F. Specific TNFR2 pathway blockade in cancer
1. Rationale
2. Pioneer approaches
TNFR2 inhibition blocks tumour growth post-alloHSCT
A. Mouse model of post-alloHSCT relapse: advantages and limitations
B. On the role of TNFR2 expression on tumour cells
C. On the risk of GvHD induction after anti-TNFR2 treatment
TNFR2 blockade spurs the alloimmune response
A. By helping effector response initiation
B. By inducing Treg stability and function decline
C. Integrative view of TNFR2 inhibition impact in alloHSCT
TNFR2 is a legitimate new ICP target of the anti-cancer arsenal
A. TNF- pathway as a promising anti-cancer agent once more
B. TNFR2 attractive pattern of expression
C. TNFR2 modulation of Teff/Treg equilibrium
D. Potential side effects for TNFR2 blockade
E. Activation versus TNFR2 blockade in tumoral context
F. Hopes for combined therapies
TRANSLATIONAL PERSPECTIVES
BIBLIOGRAPHY
