**7. Secondary vasculitis**

*6.3.2. Dacilizumab*

*6.3.3. Basiliximab*

ANCA associated vasculitis. [112]

260 Updates in the Diagnosis and Treatment of Vasculitis

Depletion of effector T cells

Regulation of effector T cells

Interference with granuloma formation

Depletion of B lymphocytes

Inhibition of B cell maturation

Antimicrobial treatment

Inhibition of migration

Enhance vascular repair

consideration for the ANCA associated vasculitis. [113, 114]

A humanized IgG1 monoclonal antibody produced by recombinant DNA technology that binds specifically to the alpha subunit (p55 alpha, CD25, or Tac subunit) of the human highaffinity interleukin-2 (IL-2) receptor that is expressed on the surface of activated lymphocytes. Dacilizumab proved to be an effective alternative in interferon refractory relapsing remitting multiple sclerosis. The drug is currently being investigated in autoimmune diseases including

A chimeric (murine/human) monoclonal antibody (IgG1K), produced by recombinant DNA technology, that functions as an immunosuppressive agent, specifically binding to and blocking the interleukin-2 receptor α-chain (IL-2Rα, also known as CD25 antigen) on the surface of activated T-lymphocytes, inhibiting the binding of IL-2 to it's receptor on target T cells. The drug is being currently used for treatment of allograft rejection and potentially under

**Principle Mechanism Agent Evidences**

Basiliximab Daclizumab

Abatacept Belatacept (CTLA-4 fusion proteins)

Infliximab Adalimumab

Rituximab Epratezumab (both are anti-CD20)

> Belimumab Atacicept

cotrimoxazole

Natalizumab

Erythropoietin (EPO) Statins

Randomized controlled trials in AAV

Randomized controlled trials in AAV

> Experimental and clinical evidences in AAV

> Experimental and clinical evidences in AAV

Experimental evidence

Experimental and clinical evidences in AAV

Experimental and clinical evidences in MS Evidences in AAV are lacking

Experimental and clinical evidence

Antibodies directed to CD25 cell surface antigen on activated T cells

Blockade of CD28/CD80 costimulatory signal for T cell activation

Tumor necrosis factor blockade

B lymphocyte depletion by antibodies directed to CD20/ CD22 cell surface molecule

Neutralization of BLys and blockade of BLys receptor on B cells

Reduction of microbial flora that might provoke disease flares

Blockade of a-4integrins on T cells

Promote epithelial progenitor cell (EPC) function and repair

**Table 3.** Current and future considerations in treat to target strategy in systemic vasculitis.[116]

The role of biologic therapy in the management of leukocytoclastic vasculitis secondary to rheumatoid arthritis, systemic lupus erythematosus and Sjogren's syndrome has not been fully explored. Anti-tumor necrosis factor (TNF) treatment proved to be effective in rheumatoid arthritis patients with refractory systemic rheumatoid vasculitis after failure of conventional therapy including cyclophosphamide and corticosteroids with successful tapering of cortico‐ steroids. The use of anti-TNF therapy and other biologic drugs might be considered in refractory secondary vasculitis to induce remission and as steroid sparing therapy for main‐ tenance of remission. [115]
